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Cited by 5MicroRNA in disease regulationPlant Molecular Biology ResearchCancer-related molecular mechanisms research

Recent advances of miR-23 in human diseases and growth development

Open access
Qian, Xu, Jiang, Yongwei, Yang, Yadi, Zhang, Yukun, Xu, Na, Xu, Bin, Pei, Ke, Yu, Zhi +1 more·2025·Non-coding RNA Research
DOI 10.1016/j.ncrna.2024.12.010PMC PMC11787465
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Abstract

MicroRNA (miRNA) is broadly manifested in eukaryotes and serves as a critical function in biological development and disease occurrence. With the rapid advancement of experimental research tools, researchers have discovered functional correlations among different miRNA isoforms and clusters within the same miRNA family. As a highly conserved member in the miR-23-27-24 cluster, miR-23 exhibits different isoforms and participates in various essential development. Although the miR-23-27-24 cluster has overlapping target sites, their differential expression can demonstrate independent biological functions. Furthermore, the untapped effects of miR-23 on organisms, whether as a functional cluster or a single regulator, has not been systematically elucidated yet. In this review article, we analyze the genomic location of miR-23 and its sequence variances among its isoforms or family members while summarizing its regulatory functions in metabolic diseases, immune responses, cardiovascular diseases, cancer, organ development as well as nervous system function. This review highlights the significant role of miR-23 as a biomarker for disease diagnosis and a key regulatory factor in pathogenesis, which can help us comprehend the diverse functions of miRNAs and provide a theoretical reference for the functional differences among miRNA isoforms.

AI snapshot

Written from the paper’s full text.

TL;DR

This review summarizes the genomic organization, isoform conservation, and regulatory roles of miR-23 across metabolic, immune, cardiovascular, cancer, organ development, and nervous system contexts. It highlights miR-23 as a potential disease biomarker and therapeutic target, while emphasizing isoform-specific and context-dependent effects.

Key findings

  • miR-23 belongs to the miR-23-27-24 cluster; human miR-23a and miR-23b are on chromosomes 19 and 9, while mouse miR-23a/b are on chromosomes 8 and 13. Mature sequences are conserved, but miR-23-3p is more conserved than miR-23-5p; miR-23b-5p is more conserved than miR-23a-5p, whereas miR-23b-3p is less conserved than miR-23a-3p.
  • In metabolic disease, miR-23 is often upregulated. For example, miR-23a-3p was decreased in serum of type 2 diabetic nephropathy patients (112 cases) and lower with increasing disease severity; antagomirs against the miR-23-27-24 cluster in neonatal mice promoted bile duct differentiation and reduced hepatocyte proliferation, inhibited fibrosis in newborn Alb/TGF-β1 transgenic mice, and restored existing fibrosis in old mice.
  • In immune and cardiovascular contexts, miR-23 regulates T cells, macrophages, and inflammation; miR-23 was downregulated in serum from patients with virus-negative inflammatory dilated cardiomyopathy (152 patients with heart failure), and miR-23-3p was reduced with increased TNF-α in obstructive sleep apnea patients (40 samples) compared with 20 primary snoring subjects.
  • In cancer and development, miR-23a/b are frequently upregulated and promote growth/metastasis in many tumors, but show context-dependent downregulation in oral squamous cell carcinoma, prostate cancer, and osteosarcoma; miR-23 also affects skeletal muscle via TrxR1, bone via Runx2/Satb2/MEF2C, tooth development via Hmgn2/Whsc1, cardiac development via Has2, reproduction via CUL3/β-catenin, and neural differentiation via Hes1.

Methods

  • Narrative review; no systematic search strategy or meta-analysis is described.
  • Analyzed miR-23 genomic location and sequence conservation across species using NCBI and miRbase data, with alignment performed in Vector NTI.
  • Summarized regulatory functions across metabolic diseases, immune responses, cardiovascular disease, cancer, organ development, and the nervous system, supported by tables of expression patterns and target genes and by cited human clinical samples, animal models, and cell experiments. No primary experiments are reported.

Limitations

  • Stated in the paper: for spinal cord injury, the study lacks relevant experimental verification; for abdominal aortic aneurysm, the observation is limited to clinical samples and lacks further mechanism investigation; for bone formation, more precise experiments are needed; and for biomarker use, more standardized guidelines are needed.
  • Stated/evident: as a narrative review, it lacks systematic search and quantitative synthesis, and conclusions rely on heterogeneous cited studies across species, models, tissues, and disease stages.
  • Evident: many target genes in the tables are listed as “unverified” or “unidentified,” and several mechanisms are inferred from animal or cell models, so clinical translation remains uncertain.

Model-written summary. Check it against the paper before relying on it.

Integrity signals

Registry

Crossref · 10.1016/j.ncrna.2024.12.010

Cites

140 of 140 references verified0 citation errors · 0 not checkable

Statistics

Nothing to recompute.

Claims the paper makes

185 of 282 cited sources checked · 59 supported · 13 flagged · accuracy not yet measured

  • Premisecitation

    The miR-23-27-24 cluster participates in endoplasmic reticulum stress within adipocytes and improves their endocrine function through targeting EDEM3.

    “This cluster participate in endoplasmic reticulum stress within adipocytes and improve their endocrine function through protease targeting ER degradation enhancing alpha-mannosidase like protein 3 (EDEM3) [23].”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites [23] Gan, 2022, Ischemic heart-derived small extracellular vesicles impair adipocyte function, Circ. Res. source

      The Discussion says the miR-23-27-24 cluster causes adipocyte ER stress and endocrine dysfunction, not improved endocrine function. The EDEM3 section identifies EDEM3 as a miR-27 target and says its suppression is responsible for that dysfunction; inhibiting miR-27 instead restored endocrine function. (LLM, conf=0.93)

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  • Premisecitation

    The miR-23-27-24 cluster coordinates control of follicular helper T cells by targeting essential gene networks, thereby promoting humoral immunity.

    “Follicular helper T cells are crucial for the generation of protective humoral immunity, and the miR-23-27-24 cluster coordinates the control of follicular helper T cells by targeting essential gene networks, thereby promoting humoral immunity [27].”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites [27] Wu, 2019, MiR-23∼27∼24-mediated control of humoral immunity reveals a TOX-driven regulatory circuit in follicular helper T cell differentiation, Sci. Adv. source

      The Results section confirms that the miR-23~27~24 family cooperatively targets genes involved in follicular helper T-cell differentiation. But it reports the opposite direction of effect: deleting the family increased follicular helper T-cell responses and virus-specific antibodies, while overexpressing it diminished follicular helper T-cell and germinal-center B-cell responses. The claim that the cluster thereby promotes humoral immunity is contrary to these findings (page unavailable in our copy). (LLM, conf=0.90)

      Checked by a reasoning model — may be wrong.

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  • Premisecitation

    Expression levels of miR-23a-3p are increased in abdominal aortic aneurysm.

    “the expression levels of miR-23a-3p are also increased in abdominal aortic aneurysm (AAA)”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites [97] Černá, 2019, The expression profile of MicroRNAs in small and large abdominal aortic aneurysms, Cardiol. Res. Pract. source

      Section 3.3 (Results) identifies miR-23a-3p among the miRNAs downregulated in large aneurysmal walls compared with healthy controls. The Abstract (Results) reports the same direction of change, contrary to the claimed increase. (LLM, conf=0.90)

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  • Premisecitation

    In melanoma and pituitary tumors, miR-23a binds to lncRNA Malat1 and MEG3.

    “in melanoma and pituitary tumors, miR-23a binds to lncRNA Malat1 and MEG3.”
    Quote in the paperNot a substantial claim2 of 2 sources checked
    • cites [100] Wang, 2020, LncRNA MALAT1 promotes the proliferation, migration, and invasion of melanoma cells by downregulating miR-23a, Cancer Manag. Res. source

      The Results section (“miR-23a is the Target Gene of lncRNA MALAT1”; page unavailable) reports sequence pairing and a luciferase assay supporting MALAT1–miR-23a binding in melanoma cells. The paper does not report this interaction with MEG3 in pituitary tumors; its References section mentions a MEG3–miR-23a study in laryngeal cancer instead. (LLM, conf=0.90)

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    • cites [101] Wang, 2021, lncRNA MEG3 inhibits pituitary tumor development by participating in cell proliferation, apoptosis and EMT processes, Oncol. Rep. source

      The Results section identifies miR-23b-3p—not miR-23a—as the molecule that binds MEG3 in the pituitary-tumor study, citing a luciferase reporter assay and RNA pull-down assay. The passages do not address binding to MALAT1 in melanoma. (LLM, conf=0.86)

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  • Premisecitation

    Hes1 is an authentic target of miR-23.

    “A basic helix-loop-helix transcriptional repressor, named Hes1, is an authentic target of miR-23.”
    Quote in the paperSubstantial claim2 of 3 sources checked
    • cites [129] Smirnova, 2005, Regulation of miRNA expression during neural cell specification, Eur. J. Neurosci. source
    • cites [130] Kawasaki, 2003, Functional analysis of microRNAs during the retinoic acid-induced neuronal differentiation of human NT2 cells, Nucleic Acids Res. Suppl. source
    • cites [131] Wang, 2010, Mouse microRNA-124 regulates the expression of Hes1 in P19 cells, Front. Biosci. source

      Section 4.3 identifies Hes-1 as a target of miR-124 in P19 cells, not miR-23. The Discussion likewise attributes the observed regulation of Hes-1 protein to miR-124. The cited paper therefore supports a different microRNA identity than the one attributed to it. (LLM, conf=0.88)

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  • May combine two claims. 106
  • Classified as probably not a substantial claim. 10
  • The quote only partly states this claim. 1

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    Premisecitation

    miR-23 targets CXCL12 to modulate the NF-κB signaling pathway, leading to decreased TNF-α, IL-1β, and IL-8 expression levels, which inhibit inflammation and enhance RA.

    “Further investigation has demonstrated that miR-23 targets C-X-C motif ligand 12 (CXCL12) to modulate the NF-κB signaling pathway, leading to decreased TNF-α, IL-1β, and IL-8 expression levels which inhibit inflammation and enhance RA.”
    Quote in the paperSubstantial claim2 of 2 sources checked
    • cites [13] Castro-Villegas, 2015, Circulating miRNAs as potential biomarkers of therapy effectiveness in rheumatoid arthritis patients treated with anti-TNFα, Arthritis Res. Ther. source

      The Results (Regulation network; page unavailable) list CHUK as a potential target of miR-23, and the Discussion (page unavailable) explains that CHUK mediates NF-κB activation. The paper does not identify CXCL12 as a miR-23 target or show that miR-23 lowers TNF-α, IL-1β, and IL-8 through that pathway; its proposed targets are not evidence of the claimed causal sequence. (LLM, conf=0.83)

      Experimental — accuracy not yet measured
    • cites [31] Gao, 2021, microRNA-23 inhibits inflammation to alleviate rheumatoid arthritis via regulating CXCL12, Exp. Ther. Med. source

      The Results report that miR-23 reduced TNF-α, IL-1β and IL-8 through CXCL12 and NF-κB signaling. But the Discussion says this inhibited inflammation to alleviate RA, contrary to the citing sentence’s claim that it would “enhance RA.” (LLM, conf=0.88)

      Checked by a reasoning model — may be wrong.

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    Premisecitation

    miR-23a can alleviate lipopolysaccharide-induced cell damage by directly binding ROCK1 to inhibit its expression; ROCK1 prevents SIRT1 expression and stimulates NF-κB phosphorylation, thereby inhibiting lipopolysaccharide-induced cell damage and inflammatory cytokine secretion.

    “as well as by directly binding Rho associated coiled-coil containing protein kinase 1 (ROCK1) to inhibit its expression level. ROCK1 prevents the expression of SIRT1 and stimulates the phosphorylation of the NF-κB signaling pathway, thereby inhibiting lipopolysaccharide-induced cell damage and inflammatory cytokine secretion [38].”
    Quote in the paperSubstantial claim1 of 1 sources checked
    • cites [38] Shi, 2021, MicroRNA-23a reduces lipopolysaccharide-induced cellular apoptosis and inflammatory cytokine production through Rho-associated kinase 1/sirtuin-1/nuclear factor-kappa B crosstalk, Chin. Med. J. source

      Split into 2 atoms — 1 confirmed, 0 partially supported, 1 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.

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    Premisecitation

    miR-23a specifically binds to p53 to stimulate its transcriptional activity in cardiomyocytes and promotes oxidative stress-induced cell apoptosis.

    “it also specifically binds to p53 to stimulate its transcriptional activity in cardiomyocytes and promotes oxidative stress-induced cell apoptosis.”
    Quote in the paperNot a substantial claim2 of 3 sources checked
    • cites [60] Li, 2023, MiR-23a-3p alleviates cigarette smoke extract-induced pulmonary vascular endothelial cell apoptosis by targeting DNAJB1 in emphysema, Clin. Res. J source

      The Discussion (page unavailable) reports the opposite effect in cardiomyocytes: miR-23a-3p overexpression alleviated high-glucose-induced apoptosis. The Results section on miR-23a-3p targeting (page unavailable) identifies DNAJB1, not p53; no passage supports p53 binding or stimulation of its transcriptional activity. (LLM, conf=0.88)

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    • cites [61] Li, 2015, miR-23a binds to p53 and enhances its association with miR-128 promoter, Sci. Rep. source
    • cites [62] Yang, 2017, The mechanism of miR-23a in regulating myocardial cell apoptosis through targeting FoxO3, Eur. Rev. Med. Pharmacol. Sci. source

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    Premisecitation

    In rats with myocardial ischemia-reperfusion injury, miR-23 can target FoxO3a to regulate cardiomyocyte growth, leading to increased cardiomyocyte apoptosis, while overexpression of miR-23 effectively reduced this phenomenon.

    “In rats with myocardial ischemia-reperfusion injury, it can target FoxO3a to regulate cardiomyocyte growth, leading to increased cardiomyocyte apoptosis while the overexpression of miR-23 effectively reduced this phenomenon [[60], [61], [62]].”
    Quote in the paperSubstantial claim2 of 3 sources checked
    • cites [60] Li, 2023, MiR-23a-3p alleviates cigarette smoke extract-induced pulmonary vascular endothelial cell apoptosis by targeting DNAJB1 in emphysema, Clin. Res. J source

      The Discussion (page unavailable) reports that miR-23a-3p overexpression alleviated high-glucose-induced cardiomyocyte apoptosis. It does not support the claim’s rat myocardial ischemia-reperfusion setting, FoxO3a target, or regulation of cardiomyocyte growth; the paper’s Results instead identify DNAJB1 as the target in pulmonary vascular endothelial cells. (LLM, conf=0.86)

      Experimental — accuracy not yet measured
    • cites [61] Li, 2015, miR-23a binds to p53 and enhances its association with miR-128 promoter, Sci. Rep. source

      The Results (page not provided) report the opposite effect: miR-23a overexpression increased cardiomyocyte susceptibility to apoptosis after hydrogen peroxide or doxorubicin treatment, while knockdown reduced apoptosis. The Methods describe cultured neonatal rat cardiomyocytes, not rats with myocardial ischemia-reperfusion injury; the Discussion identifies a p53/miR-128 pathway rather than FoxO3a. (LLM, conf=0.90)

      Checked by a reasoning model — may be wrong.

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    • cites [62] Yang, 2017, The mechanism of miR-23a in regulating myocardial cell apoptosis through targeting FoxO3, Eur. Rev. Med. Pharmacol. Sci. source

  • May combine two claims.

    Premisecitation

    Overexpression of miR-23a-3p can promote cell viability and repress apoptosis.

    “Additionally, there are certain studies explicit that overexpression of miR-23a-3p can promote cell viability as well as repressed apoptosis.”
    Quote in the paperSubstantial claim2 of 3 sources checked
    • cites [60] Li, 2023, MiR-23a-3p alleviates cigarette smoke extract-induced pulmonary vascular endothelial cell apoptosis by targeting DNAJB1 in emphysema, Clin. Res. J source
    • cites [61] Li, 2015, miR-23a binds to p53 and enhances its association with miR-128 promoter, Sci. Rep. source

      The Results section, “miR-23a participates in the regulation of apoptosis” (page not supplied), reports the opposite of the claimed effect: miR-23a overexpression sensitized cardiomyocytes to apoptosis induced by hydrogen peroxide or doxorubicin. The supplied passages do not report increased cell viability or establish that the tested miR-23a was specifically miR-23a-3p. (LLM, conf=0.90)

      Checked by a reasoning model — may be wrong.

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    • cites [62] Yang, 2017, The mechanism of miR-23a in regulating myocardial cell apoptosis through targeting FoxO3, Eur. Rev. Med. Pharmacol. Sci. source

  • May combine two claims.

    Study design and conductcitation

    The observation of increased miR-23a-3p in abdominal aortic aneurysm is limited to clinical samples and lacks further investigation of its regulation mechanism.

    “this observation is limited to clinical samples and lacks further investigation of its regulation mechanism [97].”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites [97] Černá, 2019, The expression profile of MicroRNAs in small and large abdominal aortic aneurysms, Cardiol. Res. Pract. source

      Section 3.3 (page unavailable) reports that miR-23a-3p was downregulated, not increased, in large abdominal aortic aneurysm tissue. Although this study analyzed clinical tissue samples, its reported direction of expression contradicts the observation described in the claim. (LLM, conf=0.91)

      Checked by a reasoning model — may be wrong.

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    Premisecitation

    Downregulation of Malat1 or MEG3 leads to an increase in miR-23a levels, consequently promoting tumor cell proliferation, migration, and invasion.

    “A downregulation of Malat1 or MEG3 leads to an increase in miR-23a levels, consequently promoting tumor cell proliferation, migration, and invasion [100,101].”
    Quote in the paperNot a substantial claim2 of 2 sources checked
    • cites [100] Wang, 2020, LncRNA MALAT1 promotes the proliferation, migration, and invasion of melanoma cells by downregulating miR-23a, Cancer Manag. Res. source

      The Abstract (Results; page not specified) reports that MALAT1 downregulation raises miR-23a levels but inhibits, rather than promotes, melanoma-cell proliferation, migration, and invasion. The Results section on miR-23a confirms that increasing miR-23a inhibits these behaviors. The supplied passages do not address MEG3. (LLM, conf=0.93)

      Checked by a reasoning model — may be wrong.

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    • cites [101] Wang, 2021, lncRNA MEG3 inhibits pituitary tumor development by participating in cell proliferation, apoptosis and EMT processes, Oncol. Rep. source

      The Results (page not provided) report that MEG3 knockdown increased proliferation, migration and invasion in pituitary tumor cells, and that inhibiting miR-23b-3p rescued those effects. The paper identifies the regulated microRNA as miR-23b-3p, not the claimed miR-23a; it does not study MALAT1. (LLM, conf=0.90)

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    Premisecitation

    Mutations in miRNA genes may affect miRNA biosynthesis, expression levels, 5p/3p balance, processing accuracy, and target recognition specificity.

    “Recently studies have analyzed genetic variants in miRNA genes, indicating that mutations may affect the substantial biosynthesis of miRNAs, leading to alterations in miRNA expression levels, 5p/3p miRNA balance, miRNA processing accuracy, and miRNA target recognition specificity [10].”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites [10] Machowska, 2022, Consequences of genetic variants in miRNA genes, Comput. Struct. Biotechnol. J. source

  • May combine two claims.

    Premisecitation

    In type 2 diabetic nephropathy patients (112 cases), miR-23-3p expression is decreased in serum, lower than both the control group and the simple diabetes group, and the decrease is more significant with increasing disease severity.

    “the expression level of miR-23–3p was observed to be decreased in the serum of Type 2 diabetic nephropathy (T2DN) patients (totally 112 cases), with levels being lower than both the control group and the simple diabetes group. Furthermore, this decrease was more significant with increasing severity of the disease [12,16].”
    Quote in the paperSubstantial claim1 of 2 sources checked
    • cites [12] Liu, 2021, Exosomal miR-23a and miR-192, potential diagnostic biomarkers for type 2 diabetes, Clin. Lab. source
    • cites [16] Meng, 2023, Clinical value of miR-23a-3p expression in early diagnosis of diabetic kidney disease, Endokrynol. Pol. source

      The ‘Comparison of serum miR-23a-3p levels’ section (page not specified) reports progressively lower serum levels across the control, simple-diabetes, microalbuminuria and macroalbuminuria groups. However, Table 2 (page not specified) shows 112 patients with diabetes in total, of whom 76—not 112—were in the nephropathy groups. The source also identifies the molecule as miR-23a-3p, rather than miR-23-3p. (LLM, conf=0.90)

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  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation

    miR-23, miR-27, and miR-24 can sometimes share a common target site, but their biological functions are distinct due to variations in expression regulation.

    “Sometimes, miR-23, miR-27, and miR-24 can share a common target site [9], but their biological functions are distinct due to variations in expression regulation.”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites [9] Ru, 2022, The miR-23-27-24 cluster: an emerging target in NAFLD pathogenesis, Acta Pharmacol. Sin. source

      The citation is attached to the shared-target clause. The “Interactive Functions of miR-23, miR-27, and miR-24” section reports that all three target SMAD5, but it does not establish that they bind the same target site. The later clause about distinct functions due to expression regulation is not attached to this citation. (LLM, conf=0.82)

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    Premisecitation

    Overexpression of miR-23a-3p drives proliferation of lipid-associated macrophages in obese adipose tissue and prevents diet-induced obesity metabolic dysfunction.

    “This also drives the proliferation of lipid-associated macrophages in obese adipose tissue and prevents diet-induced obesity metabolic dysfunction [21,22].”
    Quote in the paperSubstantial claim1 of 2 sources checked
    • cites [21] Li, 2021, miR-23a/b-3p promotes hepatic lipid accumulation by regulating Srebp-1c and Fas, J. Mol. Endocrinol. source
    • cites [22] Sprenkle, 2023, The miR-23-27-24 clusters drive lipid-associated macrophage proliferation in obese adipose tissue, Cell Rep. source

      The Discussion (page not provided) says that myeloid expression of the miR-23–27-24 clusters supports lipid-associated macrophage proliferation and protects against obesity-induced metabolic dysfunction. The Results (page not provided) describe deletion of the clusters, not overexpression of miR-23a-3p alone, so the specific intervention attributed to this source is unsupported. (LLM, conf=0.86)

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    Premisecitation

    miR-23a-3p can be mediated by isoglycyrrhizinate, and its expression is heightened in alcoholic liver disease.

    “Among them, miR-23a-3p can be mediated by isoglycyrrhizinate, and its expression is heightened in alcoholic liver disease.”
    Quote in the paperNot a substantial claim1 of 2 sources checked
    • cites [9] Ru, 2022, The miR-23-27-24 cluster: an emerging target in NAFLD pathogenesis, Acta Pharmacol. Sin. source

      The “MIR-24 AND MIR-23” section discusses miR-23a in NAFLD, hepatic fibrosis and steatosis, but does not link miR-23a-3p to isoglycyrrhizinate or report heightened expression in alcoholic liver disease. Searches for “isoglycyrrhizinate” and “alcoholic liver disease” found no passage establishing either part of the claim; pages were not supplied in our copy. (LLM, conf=0.73)

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    • cites [19] Wang, 2022, Isoliquiritigenin-mediated miR-23a-3p inhibition activates PGC-1α to alleviate alcoholic liver injury, Phytomedicine source

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    Premisecitation

    As a target gene of miR-23a, TGFR2 is subsequently downregulated, leading to an increase in the vitality of vascular smooth muscle cells and a reduction in cell apoptosis.

    “As a target gene of miR-23a, TGF receptor type 2 (TGFR2) is subsequently downregulated, leading to an increase in the vitality of vascular smooth muscle cells (VSMCs) and a reduction in cell apoptosis [48].”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites [48] Wu, 2021, RUNX2 promotes vascular injury repair by activating miR-23a and inhibiting TGFBR2, Ann. Transl. Med. source

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    Premisecitation

    Overexpression of miR-23 can promote the proliferation of vascular smooth muscle cells and inhibit apoptosis through the target BCL2L11.

    “Overexpression of miR-23 can promote the proliferation of VSMCs and inhibit apoptosis through another target BCL2L11 [49].”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites [49] Liu, 2018, miR-23 regulates cell proliferation and apoptosis of vascular smooth muscle cells in coronary heart disease, Pathol. Res. Pract. source

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    Premisecitation

    Expression levels of miR-23a were de-regulated in RA patient samples compared to healthy synovial tissue and serum samples, while miR-23-3p in serum was significantly upregulated by anti-TNFα/DMARDs combination therapy.

    “Clinical researches have revealed that the expression levels of miR-23a were de-regulated in RA patient samples compared to healthy synovial tissue and serum samples, while miR-23–3p in serum was significantly upregulated by anti-TNFα/DMARDs combination therapy.”
    Quote in the paperSubstantial claim2 of 2 sources checked
    • cites [13] Castro-Villegas, 2015, Circulating miRNAs as potential biomarkers of therapy effectiveness in rheumatoid arthritis patients treated with anti-TNFα, Arthritis Res. Ther. source

      The Results section, “Validation of the differentially expressed miRNAs” (page unavailable), reports that serum miR-23-3p increased significantly after anti-TNFα/DMARD combination therapy in the RA patients studied. The cited paper does not establish the claimed comparison of miR-23a expression in RA samples with healthy synovial tissue and serum samples; its reported comparison is before versus after treatment. (LLM, conf=0.88)

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    • cites [31] Gao, 2021, microRNA-23 inhibits inflammation to alleviate rheumatoid arthritis via regulating CXCL12, Exp. Ther. Med. source

      The Results (page unavailable) report significantly lower miR-23 in both serum and synovial tissue from RA patients than in healthy controls. They also state that miR-23 is upregulated after anti-TNF-α/DMARD combination therapy, but do not specify miR-23-3p, serum, or statistical significance for that treatment finding. The Introduction and Discussion instead describe miR-23 as downregulated in patients treated with anti-TNF-α. (LLM, conf=0.88)

      Experimental — accuracy not yet measured

  • May combine two claims.

    Premisecitation

    Compared with 20 matched subjects with primary snoring, miR-23-3p expression was reduced and its target gene TNF-α was increased in OSA patients (40 samples), demonstrating that miR-23-3p directly targets the TLR/TNF-α pathway to cope with chronic intermittent hypoxia with re-oxygenation injury.

    “Compared with 20 matched subjects with primary snoring (PS), the expression level of miR-23–3p was reduced and its target gene TNF-α was increased in OSA patients (40 samples), demonstrating that miR-23–3p directly targets the TLR/TNF-α pathway to cope with chronic intermittent hypoxia with re-oxygenation (IHR) injury [39].”
    Quote in the paperSubstantial claim1 of 1 sources checked
    • cites [39] Chen, 2020, miR-21-5p under-expression in patients with obstructive sleep apnea modulates intermittent hypoxia with Re-Oxygenation-Induced-Cell apoptosis and cytotoxicity by targeting pro-inflammatory TNF-α-TLR4 signaling, Int. J. Mol. Sci. source

      Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.

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    Premisecitation

    miR-23a mainly acts on permeability-related proteins, while miR-23b displays inhibition of angiogenesis by blocking cell cycle progression and reducing endothelial cell rejection signals.

    “Specifically, miR-23a mainly acts on permeability-related proteins, while miR-23b displays inhibition of angiogenesis by blocking cell cycle progression and reducing endothelial cell rejection signals [44,45].”
    Quote in the paperSubstantial claim1 of 2 sources checked
    • cites [44] Li, 2016, The poly-cistronic miR-23-27-24 complexes target endothelial cell junctions: differential functional and molecular effects of miR-23a and miR-23b, Mol. Ther. Nucleic Acids source

      The Results sections on vascular permeability and angiogenesis report that miR-23a affects endothelial junctions and permeability, while miR-23b inhibits angiogenesis. The cited passages do not establish that miR-23b does so by blocking cell-cycle progression or reducing endothelial-cell rejection signals; the paper discusses repulsive junctional proteins, but not those proposed mechanisms. Page numbers are unavailable in our copy. (LLM, conf=0.87)

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    • cites [45] Boon, 2012, Atheroprotective mechanisms of shear stress-regulated microRNAs, Thromb. Haemostasis source

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    Premisecitation

    Overexpression of miR-23a-3p inhibits the lipopolysaccharide-induced HK-2 cell proliferation inhibition, promotes apoptosis, and reduces cytokine production.

    “The overexpression of miR-23a-3p inhibits the lipopolysaccharide-induced HK-2 cell proliferation inhibition, promotes apoptosis, and reduces cytokine production.”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites [37] Ye, 2022, miR-23a-3p inhibits sepsis-induced kidney epithelial cell injury by suppressing Wnt/β-catenin signaling by targeting wnt5a, Braz. J. Med. Biol. Res. source

      The Results section reports that miR-23a-3p overexpression increased viability in LPS-treated HK-2 cells and reversed the rise in inflammatory cytokines. But it significantly attenuated apoptosis rather than promoting it. Page numbers are not provided in the supplied passages. (LLM, conf=0.92)

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    Premisecitation

    Pioglitazone modulates macrophage polarization by targeting IRF1 and Pknox1 through miR-23, transforming inflammatory M1 macrophages into anti-inflammatory M2 macrophages, reducing renal macrophage infiltration, and decreasing calcium oxalate crystal formation and renal inflammatory damage.

    “Pioglitazone modulates macrophage polarization by targeting interferon regulatory factor 1 (IRF1) and Pknox1 through miR-23, transforming inflammatory M1 type macrophages into anti-inflammatory M2 type macrophages, significantly reducing renal macrophage infiltration, thus decreasing calcium oxalate crystal formation and renal inflammatory damage [28].”
    Quote in the paperSubstantial claim1 of 1 sources checked
    • cites [28] Chen, 2019, Pioglitazone decreased renal calcium oxalate crystal formation by suppressing M1 macrophage polarization via the PPAR-γ-miR-23 axis, Am. J. Physiol. Ren. Physiol. source

  • May combine two claims.

    Premisecitation

    miR-23 was increased in mouse laser-induced choroidal neovascularization models, and suppression of miR-23 reduced choroidal neovascularization development.

    “miR-23 was increased in mouse laser-induced choroidal neovascularization models, and suppression of miR-23 reduced choroidal neovascularization development [46].”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites [46] Martinez, 2021, MicroRNAs in laser-induced choroidal neovascularization in mice and rats: their expression and potential therapeutic targets, Neural Regen Res source

      The Mouse studies section reports that miR-23a increased in mouse retina/choroid after laser injury. It also reports that an inhibitor targeting both miR-23 and miR-27 reduced CNV area; it does not establish the effect of suppressing miR-23 alone. (LLM, conf=0.85)

      Experimental — accuracy not yet measured

  • May combine two claims.

    Premisecitation

    In a sepsis mouse model, the MITF-GAS5-miR-23 positive feedback loop can alleviate vascular oxidation and inflammatory damage in sepsis and maintain vascular barrier function.

    “In a sepsis mouse model of systemic inflammatory disease induced by pathogen invasion, it was confirmed through chip PCR that the positive feedback loop, called MITF-GAS5-miR-23, which consists of miR-23 and the autophagy-related Mit-TFE transcription factor activated by oxidative stress (OS) and GAS5, can alleviate vascular oxidation and inflammatory damage in sepsis and maintain vascular barrier”
    Quote in the paperSubstantial claim1 of 1 sources checked
    • cites [35] Cheng, 2023, An autophagy-associated MITF-GAS5-miR-23 loop attenuates vascular oxidative and inflammatory damage in sepsis, Biomedicines source

      Results §3.7 reports that, in septic mice, MITF or GAS5 overexpression lowered lung ROS, stabilized endothelial junctions, and alleviated barrier dysfunction; it also reports regulation of the inflammatory response. The citing sentence overstates what ChIP-PCR established: the Abstract says ChIP-PCR confirmed transcriptional regulation of GAS5, while the protective effects were assessed in other experiments. Page numbers were not provided in our copy. (LLM, conf=0.86)

      Experimental — accuracy not yet measured

  • May combine two claims.

    Premisecitation

    Expression of miR-23a-5p in extracellular vesicles derived from M2 microglia is elevated after cerebral ischemia in mice, and it can advance white matter repair and brain function recovery after ischemic stroke by targeting Olig3.

    “On the other hand, the expression of miR-23a-5p in extracellular vesicles derived from M2 microglia is elevated after cerebral ischemia in mice, and it can advance white matter repair and brain function recovery after ischemic stroke by functioning on target gene Olig3 [66].”
    Quote in the paperSubstantial claim1 of 1 sources checked
    • cites [66] Li, 2022, M2 microglia-derived extracellular vesicles promote white matter repair and functional recovery via miR-23a-5p after cerebral ischemia in mice, Theranostics source

      The Results section (‘MiR-23a-5p was enriched in M2-EVs and enhanced oligodendrogenesis in vitro’; page not provided) reports higher miR-23a-5p in M2-EVs than M0-EVs, not an increase caused by cerebral ischemia. The Discussion (page not provided) supports a role for EV-carried miR-23a-5p in white matter repair and functional recovery after stroke, but describes mediation through Olig3 as possible rather than established. (LLM, conf=0.86)

      Experimental — accuracy not yet measured

  • May combine two claims.

    Premisecitation

    Overexpression of miR-23a can improve hypoxia/serum deprivation-induced MSC apoptosis and increase their survival rate; downregulation of miR-23 can exacerbate TNF-α-induced MSC apoptosis by regulating caspase-7.

    “Overexpression of miR-23a can improve hypoxia/serum deprivation-induced MSC apoptosis and increase their survival rate; conversely, downregulation of miR-23 can exacerbate TNF-α-induced MSC apoptosis by regulating caspase-7 [55,56].”
    Quote in the paperNot a substantial claim1 of 2 sources checked
    • cites [55] Nie, 2011, Identification of MicroRNAs involved in hypoxia- and serum deprivation-induced apoptosis in mesenchymal stem cells, Int. J. Biol. Sci. source

      The Results and Discussion section reports that overexpressing miR-23a promoted MSC survival under hypoxia and serum deprivation. It also reports that miR-23a knockdown increased apoptosis under those conditions, but does not establish the sentence’s separate claim about TNF-α-induced apoptosis or regulation of caspase-7. (LLM, conf=0.87)

      Experimental — accuracy not yet measured
    • cites [56] Mao, 2014, MicroRNA-23a is involved in tumor necrosis factor-α induced apoptosis in mesenchymal stem cells and myocardial infarction, Exp. Mol. Pathol. source

  • May combine two claims.

    Premisecitation

    In hepatocellular carcinoma, miR-23a/b are most probably derived from adipocytes and are upregulated.

    “miR-23a/b are most probably derived from adipocytes and are upregulated.”
    Quote in the paperSubstantial claim2 of 3 sources checked
    • cites [70] Liu, 2019, Adipose-derived exosomes deliver miR-23a/b to regulate tumor growth in hepatocellular cancer by targeting the VHL/HIF axis, J. Physiol. Biochem. source
    • cites [71] Kutay, 2006, Downregulation of miR-122 in the rodent and human hepatocellular carcinomas, J. Cell. Biochem. source

      The Results (Table I; page unavailable) report that miR-23a and miR-23b were upregulated in three rat hepatocellular carcinomas. The paper does not support the claim that they are probably derived from adipocytes, and its human-tumor analysis addresses miR-122 rather than miR-23a/b. (LLM, conf=0.90)

      Experimental — accuracy not yet measured
    • cites [72] Anwar, 2017, hsa-mir-183 is frequently methylated and related to poor survival in human hepatocellular carcinoma, World J. Gastroenterol. source

      The Results section ('Upregulated miRNAs after DNMT knockdown'; page not specified) reports that the hsa-miR-23 cluster was upregulated in HCC cell lines after DNMT knockdown. It does not identify miR-23a/b specifically, establish upregulation in HCC generally, or suggest an adipocyte origin. (LLM, conf=0.82)

      Experimental — accuracy not yet measured

  • May combine two claims.

    Premisecitation

    In HBV-infected HCC patients, miR-23a is decreased and target gene CCL22 is increased.

    “miR-23a decreased in HCC patients infected with the hepatitis B virus, along with an increase in the target gene CCL22.”
    Quote in the paperSubstantial claim2 of 2 sources checked
    • cites [74] Xu, 2016, Bioinformatics analysis of hepatitis C virus genotype 2a-induced human hepatocellular carcinoma in Huh7 cells, OncoTargets Ther. source

      The Conclusion (page unavailable) identifies MSMO1 as a target of miR-23a in a hepatitis C virus–infected Huh7 cell analysis. Searches for HBV-infected HCC patients, decreased miR-23a, and increased CCL22 found no passage addressing the claimed patient finding. (LLM, conf=0.76)

      Experimental — accuracy not yet measured
    • cites [75] Li, 2020, p65/miR-23a/CCL22 axis regulated regulatory T cells recruitment in hepatitis B virus positive hepatocellular carcinoma, Cancer Med. source

  • May combine two claims.

    Premisecitation

    miR-23a-3p enhances phosphorylated AKT and PD-L1 in macrophages and inhibits T cell function via the miR-23a-PTEN-AKT pathway.

    “Subsequently, it enhances the expression of phosphorylated AKT and PD-L1 in macrophages and inhibits T cell function by functioning on the miR-23a-PTEN-AKT pathway [77].”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites [77] Liu, 2019, Endoplasmic reticulum stress causes liver cancer cells to release exosomal miR-23a-3p and up-regulate programmed death ligand 1 expression in macrophages, Hepatology source

  • May combine two claims.

    Premisecitation

    In tumor tissues of 50 ovarian cancer patients, expression levels of miR-23a/b were not identical in relation to clinical pathological parameters and prognosis, suggesting functional divergence among family members.

    “in the tumor tissues of 50 patients with ovarian cancer (OC), researchers found that the expression levels of miR-23a/b were not identical in relation to the clinical pathological parameters and prognosis, suggesting there is a functional divergence among different family members.”
    Quote in the paperSubstantial claim1 of 1 sources checked
    • cites [86] Su, 2018, Correlation analysis on the expression levels of microRNA-23a and microRNA-23b and the incidence and prognosis of ovarian cancer, Oncol. Lett. source

  • May combine two claims.

    Premisecitation

    miR-23a activates Wnt/β-catenin signaling by targeting its inhibitors and promotes silencing of tumor suppressor genes by affecting DNA methylation-related genes.

    “miR-23a activates the Wnt/β-catenin signaling pathway by targeting its inhibitors and promotes the silencing of tumor suppressor genes by affecting the expression of DNA methylation-related genes [91].”
    Quote in the paperSubstantial claim1 of 1 sources checked
    • cites [91] Fan, 2022, The miR-23a/27a/24-2 cluster promotes postoperative progression of early-stage non-small cell lung cancer, Mol Ther Oncolytics source

      The Results and Discussion (page not provided) link the miR-23a/27a/24-2 cluster to suppression of Wnt/β-catenin inhibitors and to DNA methylation-related downregulation of tumor suppressor genes in NSCLC. The citing sentence attributes both effects to miR-23a alone, whereas the paper emphasizes the combined action of all three miRNAs; the Results state that only their combined overexpression produced the simultaneous changes in methylation-related genes and tumor suppressors. (LLM, conf=0.88)

      Experimental — accuracy not yet measured

  • May combine two claims.

    Premisecitation

    Overexpression of the miR-23 functional cluster accelerates tumor growth, whereas recovery of HIC1 can significantly inhibit tumor growth.

    “overexpression of the miR-23 functional cluster accelerates tumor growth, whereas the recovery of HIC1 can significantly inhibit tumor growth [82].”
    Quote in the paperSubstantial claim1 of 1 sources checked
    • cites [82] Wang, 2017, HIC1 and miR-23∼27∼24 clusters form a double-negative feedback loop in breast cancer, Cell Death Differ. source

  • May combine two claims.

    Premisecitation

    Expression level of miR-23a displayed an abnormal decrease in prostate cancer cell lines, opposite to breast and ovarian cancers.

    “The expression level of miR-23a displayed an abnormal decrease in this cancer cell lines, which is opposite to we mentioned previously in breast and ovarian cancers [88].”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites [88] Cai, 2015, Downregulation of microRNA-23a suppresses prostate cancer metastasis by targeting the PAK6-LIMK1 signaling pathway, Oncotarget source

  • May combine two claims.

    Premisecitation

    Members of the miR-23a functional cluster are overexpressed in tumors and associated with an increased risk of postoperative recurrence in non-small cell lung cancer patients.

    “members of the miR-23a functional cluster are overexpressed in tumors and associated with an increased risk of postoperative recurrence in non-small cell lung cancer (NSCLC) patients.”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites [91] Fan, 2022, The miR-23a/27a/24-2 cluster promotes postoperative progression of early-stage non-small cell lung cancer, Mol Ther Oncolytics source

      The Results (Figure 1 and the accompanying text) report that simultaneous high expression of miR-23a, miR-27a, and miR-24-2 in primary tumors was associated with postoperative recurrence. The study concerns early-stage NSCLC, however, and its recurrence finding is for high expression of all three together, not necessarily each member independently across all NSCLC patients. (LLM, conf=0.84)

      Experimental — accuracy not yet measured

  • May combine two claims.

    Premisecitation

    Expression of miR-23a is restrained by the p65 subunit of NF-κB, confirming that miR-23a is a hub for regulating glutamine metabolism.

    “the expression of miR-23a is restrained by the p65 subunit of NF-κB, confirms that miR-23a is a hub for regulating glutamine metabolism”
    Quote in the paperNot a substantial claim1 of 2 sources checked
    • cites [94] Rathore, 2012, The NF-κB member p65 controls glutamine metabolism through miR-23a, Int. J. Biochem. Cell Biol. source
    • cites [95] Khan, 2016, Human leukemic cells performing oxidative phosphorylation (OXPHOS) generate an antioxidant response independently of reactive oxygen species (ROS) production, EBioMedicine source

      The Discussion (page unavailable) links miR-23a levels to glutamine metabolism, supporting its regulatory role. But the Results section on miR-23a upregulation identifies ERK5 acting through MEF2; our copy does not establish that NF-κB p65 restrains miR-23a expression. The References list a separate Rathore et al. (2012) paper on p65 and glutamine metabolism, but this paper relies on that work when discussing miR-23a rather than merely mentioning it. (LLM, conf=0.84)

      Experimental — accuracy not yet measured

  • May combine two claims.

    Premisecitation

    Unlike the functional differentiation of miR-23a/miR-23b in ovarian cancer, their expression levels are upregulated in radiation-induced thymic lymphoma model mice and share a common target gene Fas.

    “Unlike the functional differentiation of miR-23a/miR-23b in OC, their expression levels are upregulated in radiation-induced thymic lymphoma model mice and share a common target gene Fas.”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites [96] Li, 2013, Up-regulated expression of miR-23a/b targeted the pro-apoptotic Fas in radiation-induced thymic lymphoma, Cell. Physiol. Biochem. source

  • May combine two claims.

    Premisecitation

    miR-23a was induced under hypoxic circumstances and can act upon pro-apoptotic signals to promote tumor formation and oncogenic transformation.

    “miR-23a was induced under hypoxic circumstances and can ultimately act upon pro-apoptotic signals to promote tumor formation and oncogenic transformation [89].”
    Quote in the paperSubstantial claim1 of 1 sources checked
    • cites [89] Kulshreshtha, 2007, A microRNA signature of hypoxia, Mol. Cell Biol. source

      The Results table reports increased miR-23a expression under hypoxia. The Discussion predicts that miR-23 targets pro-apoptotic components, but the paper does not demonstrate this effect for miR-23a or show that it promotes tumor formation or oncogenic transformation. The Results report caspase inhibition for miR-26, miR-107, and miR-210 instead. (LLM, conf=0.90)

      Experimental — accuracy not yet measured

  • May combine two claims.

    Premisecitation

    The miR-23a functional cluster can affect antioxidant response elements by targeting KEAP1, participates in oxidative phosphorylation of tumor cells, and affects mitochondrial activity.

    “the miR-23a functional cluster can affect antioxidant response elements by targeting KEAP1, participates in oxidative phosphorylation of tumor cells, and affects mitochondrial activity [94,95].”
    Quote in the paperNot a substantial claim1 of 2 sources checked
    • cites [94] Rathore, 2012, The NF-κB member p65 controls glutamine metabolism through miR-23a, Int. J. Biochem. Cell Biol. source
    • cites [95] Khan, 2016, Human leukemic cells performing oxidative phosphorylation (OXPHOS) generate an antioxidant response independently of reactive oxygen species (ROS) production, EBioMedicine source

  • May combine two claims.

    Premisecitation

    lncRNA LINC00909 is upregulated in tumor and serum tissues and adsorbs miR-23a-3p, promoting epithelial-mesenchymal transition in ovarian cancer cells.

    “The lncRNA LINC00909 is upregulated in the tumor and serum tissues and adsorbs miR-23a-3p, thereby promoting epithelial-mesenchymal transition (EMT) in OC cells”
    Quote in the paperSubstantial claim1 of 1 sources checked
    • cites [87] Yang, 2021, Elevated LINC00909 promotes tumor progression of ovarian cancer via regulating the miR-23b-3p/MRC2 Axis, Oxid. Med. Cell. Longev. source

      The Introduction and Discussion report elevated LINC00909 in ovarian tumor and serum specimens and say it promotes EMT by sponging miR-23b-3p. The claim names miR-23a-3p instead; our copy does not support that target. (LLM, conf=0.92)

      Experimental — accuracy not yet measured

  • May combine two claims.

    Premisecitation

    Over-expression of miR-23a reduces expression of its target glutaminase GLS, induces mitochondrial dysfunction, and leads to leukemia cell death.

    “over-expression of miR-23a reduces the expression of its target glutaminase GLS, induces mitochondrial dysfunction, and leads to leukemia cell death”
    Quote in the paperSubstantial claim1 of 2 sources checked
    • cites [94] Rathore, 2012, The NF-κB member p65 controls glutamine metabolism through miR-23a, Int. J. Biochem. Cell Biol. source
    • cites [95] Khan, 2016, Human leukemic cells performing oxidative phosphorylation (OXPHOS) generate an antioxidant response independently of reactive oxygen species (ROS) production, EBioMedicine source

      The Discussion states that high miR-23a levels induce cell death through impaired glutamine metabolism and mitochondrial activity. It does not state that miR-23a overexpression reduces GLS expression; the Results instead identify KEAP1 as a direct miR-23a target. Our copy therefore supports the mitochondrial and cell-death portions, but not the specific GLS mechanism. (LLM, conf=0.86)

      Experimental — accuracy not yet measured

  • May combine two claims.

    Premisecitation

    miR-23 regulates vitamin D receptor activity, significantly influences breast cancer development, and modulates drug resistance during treatment in triple-negative breast cancer.

    “it has been found to regulate vitamin D receptor (VDR) activity, significantly influence breast cancer development, and modulate drug resistance during treatment [84,85].”
    Quote in the paperSubstantial claim2 of 2 sources checked
    • cites [84] Singh, 2017, The regulatory role of miRNAs on VDR in breast cancer, Transcription source

      The Abstract identifies miR-23 as a possible regulator of VDR activity and breast cancer development, not an established or significant influence. The section “Epigenetic control of VDR expression” says miR-23 has an oncogenic correlation but “not yet” a correlation with VDR regulation. The cited passages do not support the claim that miR-23 modulates drug resistance during TNBC treatment. (LLM, conf=0.85)

      Experimental — accuracy not yet measured
    • cites [85] Singh, 2023, Breast cancer: miRNAs monitoring chemoresistance and systemic therapy, Front. Oncol. source

      In “Role of miRNA in BC drug resistance” (page not specified), the paper links exosomes carrying miR-23a to resistance transmission in docetaxel-resistant MCF-7 breast cancer cells. It does not say that miR-23 regulates vitamin D receptor activity or significantly influences breast cancer development, and the miR-23a passage concerns MCF-7 cells rather than triple-negative breast cancer. (LLM, conf=0.86)

      Experimental — accuracy not yet measured

  • May combine two claims.

    Premisecitation

    All members of the miR-23-27-24 cluster are increased and act as oncogenes in breast cancer.

    “all members of the miR-23-27-24 cluster are increased and act as oncogenes in breast cancer.”
    Quote in the paperSubstantial claim1 of 1 sources checked
    • cites [82] Wang, 2017, HIC1 and miR-23∼27∼24 clusters form a double-negative feedback loop in breast cancer, Cell Death Differ. source

  • May combine two claims.

    Premisecitation

    High expression of miR-23a and low expression of miR-23b both determine the occurrence and progression of ovarian cancer.

    “the high expression of miR-23a and the low expression of miR-23b both determine the occurrence and progression of OC [86].”
    Quote in the paperSubstantial claim1 of 1 sources checked
    • cites [86] Su, 2018, Correlation analysis on the expression levels of microRNA-23a and microRNA-23b and the incidence and prognosis of ovarian cancer, Oncol. Lett. source

      The Results report higher miR-23a and lower miR-23b expression in ovarian tumors and associations with differentiation, lymph-node metastasis, and clinical stage. The Abstract says these expression patterns are ‘closely correlated’ with occurrence and development; it does not establish that they determine either one. Page numbers were not provided in our copy. (LLM, conf=0.88)

      Experimental — accuracy not yet measured

  • May combine two claims.

    Premisecitation

    Elevation of β-catenin and methylation of the p16 and CDH13 promoters have been linked to this over-expression.

    “The elevation of β-catenin and the methylation of the p16 and CDH13 promoters have also been linked to this over-expression.”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites [91] Fan, 2022, The miR-23a/27a/24-2 cluster promotes postoperative progression of early-stage non-small cell lung cancer, Mol Ther Oncolytics source

  • May combine two claims.

    Interpretationcitation

    The impact of miR-23 on organisms is long-lasting and can affect tooth growth during embryonic stages.

    “The studies provide evidences that the impact of miR-23 on organisms is long-lasting and can affect tooth growth during embryonic stages.”
    Quote in the paperSubstantial claim2 of 2 sources checked
    • cites [118] Eliason, 2022, HMGN2 represses gene transcription via interaction with transcription factors Lef-1 and Pitx2 during amelogenesis, J. Biol. Chem. source

      The Results section (Fig. 6C; page unavailable) examines embryonic mouse mandibles and links increasing miR-23a/b expression with changes associated with tooth development. The Discussion says miR-23 permits dental epithelial differentiation, but the paper does not establish a long-lasting effect on organisms or directly demonstrate altered embryonic tooth growth. (LLM, conf=0.84)

      Experimental — accuracy not yet measured
    • cites [119] Su, 2023, Wolf-Hirschhorn syndrome candidate 1 (Whsc1) methyltransferase signals via a Pitx2-miR-23/24 axis to effect tooth development, J. Biol. Chem. source

      The Results section (page unavailable) reports that miR-23a/b expression increases across embryonic stages of mouse tooth development and suggests that it regulates Whsc1 during that period. The Discussion (page unavailable) also describes a role for miR-23a/b in tooth-cell differentiation. Neither passage establishes a long-lasting effect on organisms, so that part of the claim is unsupported. (LLM, conf=0.86)

      Experimental — accuracy not yet measured

  • May combine two claims.

    Premisecitation

    miR-23a/b are highly expressed in mature tooth germ, and they share common target genes Hmgn2 and Whsc1.

    “miR-23a/b are highly expressed in mature tooth germ, and they share common target genes, namely high mobility group protein N2 (Hmgn2), and Wolf-Hirschhorn syndrome candidate 1 gene (Whsc1).”
    Quote in the paperNot a substantial claim2 of 2 sources checked
    • cites [118] Eliason, 2022, HMGN2 represses gene transcription via interaction with transcription factors Lef-1 and Pitx2 during amelogenesis, J. Biol. Chem. source

      The Results sections report that miR-23a and miR-23b increase at later stages of mouse tooth development and that both target and repress Hmgn2. The paper does not identify Whsc1 as a target of either miRNA, so the claim that they share both named targets is unsupported. (LLM, conf=0.89)

      Experimental — accuracy not yet measured
    • cites [119] Su, 2023, Wolf-Hirschhorn syndrome candidate 1 (Whsc1) methyltransferase signals via a Pitx2-miR-23/24 axis to effect tooth development, J. Biol. Chem. source

  • May combine two claims.

    Premisecitation

    The abundance of miR-23a functional clusters expressed in skeletal muscle is not stable enough, and mice lacking this functional cluster quickly downregulate the expression level of mature miR-23a.

    “the abundance of miR-23a functional clusters expressed in skeletal muscle is not stable enough, and mice lacking this functional cluster quickly downregulate the expression level of mature miR-23a [107,108].”
    Quote in the paperNot a substantial claim2 of 2 sources checked
    • cites [107] Ding, 2022, Identification of miRNA-mRNA networks associated with pigeon skeletal muscle development and growth, Animals source

      The Results (§3.6) identify miR-23-y as a hub miRNA in pigeon skeletal muscle, but do not address miR-23a functional-cluster stability or mice lacking that cluster. Searches for miR-23a and cluster knockout effects found no passage reporting a decline in mature miR-23a. (LLM, conf=0.76)

      Experimental — accuracy not yet measured
    • cites [108] Oikawa, 2023, Skeletal muscle-enriched miRNAs are highly unstable in vivo and may be regulated in a Dicer-independent manner, FEBS J. source

  • May combine two claims.

    Premisecitation

    There existed no notable variance in the number of osteoblasts and osteoclasts between miR-23 transgenic and wild-type mice, along with their activity in bone.

    “there existed no notable variance in the number of osteoblasts and osteoclasts between miR-23 transgenic and wild-type mice, along with their activity in the bone.”
    Quote in the paperSubstantial claim2 of 2 sources checked
    • cites [109] Zhang, 2011, A program of microRNAs controls osteogenic lineage progression by targeting transcription factor Runx2, Proc. Natl. Acad. Sci. U. S. A. source

      The Results section reports miR-23a effects on osteoblast cell cultures, including reduced ALP activity, but does not compare miR-23 transgenic mice with wild-type mice. Searches for that comparison and for osteoclast numbers or activity found no passage addressing the claim. (LLM, conf=0.75)

      Experimental — accuracy not yet measured
    • cites [110] Park, 2015, The microRNA-23a has limited roles in bone formation and homeostasis in vivo, Physiol. Res. source

  • May combine two claims.

    Premisecitation

    Human hemoglobin combined with vesicles-derived miR-23a-3p overexpression through gel scaffold can repair and reconstruct bone through the PTEN/AKT signal pathway, and promote osteogenesis and angiogenesis.

    “Human hemoglobin combined with vesicles-derived miR-23a-3p overexpression through gel scaffold can repair and reconstruct bone through PTEN/AKT signal pathway, and promote osteogenesis and angiogenesis [[111], [112], [113]].”
    Quote in the paperSubstantial claim3 of 3 sources checked
    • cites [111] Russo, 2021, MiRNAs expression profiling in Raw264.7 macrophages after nfatc1-knockdown elucidates potential pathways involved in osteoclasts differentiation, Biology source

      The Discussion (page unavailable) reports that miR-23a-3p is highly expressed in exosomes from RANKL-induced RAW264.7 cells and was downregulated after NFATc1 silencing. It does not report a hemoglobin–gel scaffold treatment, bone repair, osteogenesis, angiogenesis, or a PTEN/AKT mechanism. (LLM, conf=0.82)

      Experimental — accuracy not yet measured
    • cites [112] Hu, 2020, miR-23a-3p-abundant small extracellular vesicles released from Gelma/nanoclay hydrogel for cartilage regeneration, J. Extracell. Vesicles source

      The Results section reports that vesicle-delivered miR-23a-3p targets PTEN and activates AKT signalling; the Discussion reports cartilage regeneration using a Gelma/nanoclay hydrogel. The paper does not report a human-hemoglobin combination, bone reconstruction, osteogenesis, or angiogenesis. Page numbers were not provided in our copy. (LLM, conf=0.89)

      Experimental — accuracy not yet measured
    • cites [113] Hu, 2022, Small extracellular vesicles released from bioglass/hydrogel scaffold promote vascularized bone regeneration by transferring miR-23a-3p, Int. J. Nanomed. source

      The Conclusions (page unavailable) report that small extracellular vesicles from human umbilical cord mesenchymal stem cells delivered miR-23a-3p, promoted osteogenesis and angiogenesis through PTEN/AKT signaling in vitro, and that a bioglass/hydrogel scaffold releasing the vesicles achieved vascularized bone regeneration. The source does not describe human hemoglobin as a component or establish that miR-23a-3p was overexpressed in the scaffold; its in vivo bone-repair finding and in vitro pathway finding are distinct. (LLM, conf=0.89)

      Experimental — accuracy not yet measured

  • May combine two claims.

    Premisecitation

    During human cartilage regeneration, expression level of miR-23a-3p in small extracellular vesicles derived from umbilical cord mesenchymal stem cells was significantly ramped up, inhibiting PTEN.

    “during human cartilage regeneration, the expression level of miR-23a-3p in small extracellular vesicles derived from umbilical cord mesenchymal stem cells was significantly ramped up, inhibiting the expression level of PTEN.”
    Quote in the paperSubstantial claim3 of 3 sources checked
    • cites [111] Russo, 2021, MiRNAs expression profiling in Raw264.7 macrophages after nfatc1-knockdown elucidates potential pathways involved in osteoclasts differentiation, Biology source

      The Discussion (page unavailable) discusses miR-23a-3p in exosomes from RANKL-induced RAW264.7 cells and reports its downregulation after NFATc1 silencing. It does not address human cartilage regeneration, vesicles from umbilical-cord mesenchymal stem cells, or PTEN; searches for those terms found no relevant passage in our copy. (LLM, conf=0.77)

      Experimental — accuracy not yet measured
    • cites [112] Hu, 2020, miR-23a-3p-abundant small extracellular vesicles released from Gelma/nanoclay hydrogel for cartilage regeneration, J. Extracell. Vesicles source

      The Results section reports that vesicles from human umbilical cord mesenchymal stem cells delivered miR-23a-3p into chondrocytes and human bone marrow mesenchymal stem cells, where miR-23a-3p increased and PTEN decreased. It does not report that miR-23a-3p expression increased within the vesicles during human cartilage regeneration; its microarray finding is that miR-23a-3p was the most highly expressed miRNA in those vesicles. (LLM, conf=0.88)

      Experimental — accuracy not yet measured
    • cites [113] Hu, 2022, Small extracellular vesicles released from bioglass/hydrogel scaffold promote vascularized bone regeneration by transferring miR-23a-3p, Int. J. Nanomed. source

      The Results section reports that hUC-MSC-derived sEVs significantly increased miR-23a-3p in recipient cells and decreased PTEN expression. The study examines osteogenesis and angiogenesis during bone regeneration, not an increase in vesicle miR-23a-3p during human cartilage regeneration. It mentions cartilage repair only as a finding of a previous study. (LLM, conf=0.88)

      Experimental — accuracy not yet measured

  • May combine two claims.

    Premisecitation

    In a genome-wide analysis of ovarian miRNA expression profiles in humans, mice, cows, pigs, goats, and other mammals, the miR-23 functional cluster is upregulated in human ovarian follicles, showing species specificity, which assumes a part in follicular atresia and promotes granulosa cell apoptosis.

    “In a genome-wide analysis of ovarian miRNA expression profiles in humans, mice, cows, pigs, goats, and other mammals, the miR-23 functional cluster is upregulated in human ovarian follicles, showing species specificity, which assumes a part in follicular atresia and promotes granulosa cell apoptosis [123].”
    Quote in the paperSubstantial claim1 of 1 sources checked
    • cites [123] Zhang, 2019, MicroRNAs in ovarian follicular atresia and granulosa cell apoptosis, Reprod. Biol. Endocrinol. source

      Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.

      Experimental — accuracy not yet measured

  • May combine two claims.

    Premisecitation

    miR-23a and miR-23b share a common target and have consistent functions, affecting skeletal muscle differentiation by inhibiting TrxR1 and participating in skeletal muscle generation.

    “miR-23a and miR-23b share a common target and have consistent functions, which can affect skeletal muscle differentiation by inhibiting Thioredoxin reductase 1 (TrxR1) and participate in skeletal muscle generation [[104], [105], [106]].”
    Quote in the paperNot a substantial claim3 of 3 sources checked
    • cites [104] Pessôa, 2019, Generation and miRNA characterization of equine induced pluripotent stem cells derived from fetal and adult multipotent tissues, Stem Cell. Int. source

      The Results (section 3.3, page unavailable) report that equine miR-23a and miR-23b were both downregulated in induced pluripotent stem cells. Our copy does not address whether they share a target, inhibit TrxR1, or affect skeletal muscle differentiation; searches for TrxR1 and skeletal muscle differentiation found no supporting passage. (LLM, conf=0.72)

      Experimental — accuracy not yet measured
    • cites [105] Szmatoła, 2022, Assessment and distribution of runs of homozygosity in horse breeds representing different utility types, Animals source

      The Discussion (section 4.2, page not provided) identifies miR-23a and miR-23b as members of paralogous clusters and reports that members of those clusters have roles in skeletal muscle development. It does not say that miR-23a and miR-23b share a target, have consistent functions, or affect differentiation by inhibiting TrxR1; searches for TrxR1 and a shared target found no such passage. (LLM, conf=0.84)

      Experimental — accuracy not yet measured
    • cites [106] Mercatelli, 2017, MiR-23-TrxR1 as a novel molecular axis in skeletal muscle differentiation, Sci. Rep. source

  • May combine two claims.

    Premisecitation

    In horse cell reprogramming, miR-23 expression level was decreased in induced pluripotent stem cells, which can recognize breed characteristics of horses.

    “the expression level of miR-23 was decreased in induced pluripotent stem cells (iPSCs), which can recognize the breed characteristics of horses.”
    Quote in the paperNot a substantial claim3 of 3 sources checked
    • cites [104] Pessôa, 2019, Generation and miRNA characterization of equine induced pluripotent stem cells derived from fetal and adult multipotent tissues, Stem Cell. Int. source

      The Results (section 3.3.2; page not provided) report that miR-23a was downregulated in equine iPSCs derived from umbilical-cord cells relative to the source cells. The paper does not say that miR-23 expression can identify horse breed characteristics; its discussion of breed concerns possible differences in cell proliferation rates (section 4.1). (LLM, conf=0.88)

      Experimental — accuracy not yet measured
    • cites [105] Szmatoła, 2022, Assessment and distribution of runs of homozygosity in horse breeds representing different utility types, Animals source

      The Discussion (§4.2, page unavailable) reports that miR-23 expression decreased during muscle atrophy and identifies eca-miR-23a in genomic regions shared by five horse breeds. It does not report a decrease during cell reprogramming or in induced pluripotent stem cells, nor establish miR-23 as a way to recognize breed characteristics. (LLM, conf=0.85)

      Experimental — accuracy not yet measured
    • cites [106] Mercatelli, 2017, MiR-23-TrxR1 as a novel molecular axis in skeletal muscle differentiation, Sci. Rep. source

      The Results describe miR-23 experiments in C2C12 mouse myoblasts, and the Methods describe mouse muscle cells; no page numbers are provided in our copy. Searches for horse cell reprogramming, induced pluripotent stem cells, and breed characteristics found no passage addressing a decrease in miR-23 in horse iPSCs or their ability to identify breeds. (LLM, conf=0.76)

      Experimental — accuracy not yet measured

  • May combine two claims.

    Premisecitation

    miR-23 is involved in the mechanism of spermatogenesis and can regulate male reproductive function.

    “miR-23 is also involved in the mechanism of spermatogenesis and can regulate male reproductive function.”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites [128] Kasimanickam, 2014, Dysregulated microRNA clusters in response to retinoic acid and CYP26B1 inhibitor induced testicular function in dogs, PLoS One source

      The Results and Discussion (page unavailable) report that canine miR-23a and miR-23b were significantly up-regulated after retinoic-acid intervention in testes, supporting an association with a spermatogenesis-related pathway. The paper does not establish that miR-23 regulates spermatogenesis or male reproductive function; it presents the regulatory roles of individual miRNAs as needing further elucidation. (LLM, conf=0.86)

      Experimental — accuracy not yet measured

  • May combine two claims.

    Premisecitation

    Levels of miR-23 declined in the cerebellum of transgenic mice with α1ACT overexpression, confirming its function on neurogenesis and development promotion of dendritic synapses via MAPK signaling and cell death pathways, and controls the balance between cerebellar neuronal proliferation, differentiation, and cell death.

    “the levels of miR-23 declined in the cerebellum of transgenic mice with α1ACT overexpression, confirming its function on the neurogenesis and development promotion of dendritic synapses via MAPK signaling and cell death pathways, and controls the balance between cerebellar neuronal proliferation, differentiation, and cell death [132].”
    Quote in the paperSubstantial claim1 of 1 sources checked
    • cites [132] Wei, 2023, The transcription factor, α1ACT, acts through a MicroRNA network to regulate neurogenesis and cell death during neonatal cerebellar development, Cerebellum source

      Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.

      Experimental — accuracy not yet measured

  • May combine two claims.

    Premisecitation

    Hes1 is also directly targeted by miR-124, and knockdown of miR-124 levels mediated by locked nucleic acids is similar to the effect of miR-23 inhibition.

    “Hes1 is also directly targeted by miR-124, and the knockdown of miR-124 levels mediated by locked nucleic acids is similar to the effect of miR-23 inhibition.”
    Quote in the paperSubstantial claim2 of 3 sources checked
    • cites [129] Smirnova, 2005, Regulation of miRNA expression during neural cell specification, Eur. J. Neurosci. source
    • cites [130] Kawasaki, 2003, Functional analysis of microRNAs during the retinoic acid-induced neuronal differentiation of human NT2 cells, Nucleic Acids Res. Suppl. source

      The Results and Discussion (page unavailable in our copy) report that inhibiting miR-23 with synthetic siRNA increased Hes1 protein and impeded neuronal differentiation. The paper does not report that miR-124 directly targets Hes1, or test locked-nucleic-acid knockdown of miR-124 against the effect of miR-23 inhibition. (LLM, conf=0.88)

      Experimental — accuracy not yet measured
    • cites [131] Wang, 2010, Mouse microRNA-124 regulates the expression of Hes1 in P19 cells, Front. Biosci. source

      Section 4.2 reports that locked nucleic acids reduced miR-124 in differentiated P19 cells and increased Hes-1 protein; section 4.3 identifies partial sequence complementarity and says Hes-1 may be a miR-124 target. The paper does not establish direct targeting definitively, and it does not compare the effect with miR-23 inhibition. Page numbers are unavailable in our copy. (LLM, conf=0.87)

      Experimental — accuracy not yet measured

  • May combine two claims.

    Premisecitation

    miR-23 is specifically expressed in astrocytes of the adult brain and is one of the miRNAs highly expressed in neurons during brain development.

    “miR-23 is specifically expressed in astrocytes of the adult brain and is one of the miRNAs that are highly expressed in neurons during brain development.”
    Quote in the paperNot a substantial claim2 of 3 sources checked
    • cites [129] Smirnova, 2005, Regulation of miRNA expression during neural cell specification, Eur. J. Neurosci. source
    • cites [130] Kawasaki, 2003, Functional analysis of microRNAs during the retinoic acid-induced neuronal differentiation of human NT2 cells, Nucleic Acids Res. Suppl. source

      The Results and Discussion describe miR-23’s role in retinoic acid-induced differentiation of human NT2 cells, not its expression in brain cell types. Searches for adult-brain astrocytes and highly expressing neurons during brain development found no passage addressing either claim; the copy provides no page numbers. (LLM, conf=0.76)

      Experimental — accuracy not yet measured
    • cites [131] Wang, 2010, Mouse microRNA-124 regulates the expression of Hes1 in P19 cells, Front. Biosci. source

      The Introduction (page unavailable) discusses brain-expressed miRNAs induced during P19-cell differentiation, but does not identify miR-23 among them. Searches for miR-23, adult-brain astrocytes, and neuronal expression during brain development found no passage addressing the claim; the Discussion instead concerns miR-124. (LLM, conf=0.75)

      Experimental — accuracy not yet measured

  • May combine two claims.

    Premisecitation

    Decrease in miR-23 levels can lead to accumulation of Hes1 during retinal acid-induced neural differentiation in NT2 cells, which in turn affects neural differentiation.

    “The decrease in miR-23 levels can lead to the accumulation of Hes1 during retinal acid-induced neural differentiation in NT2 cells, which in turn affects neural differentiation.”
    Quote in the paperSubstantial claim2 of 3 sources checked
    • cites [129] Smirnova, 2005, Regulation of miRNA expression during neural cell specification, Eur. J. Neurosci. source
    • cites [130] Kawasaki, 2003, Functional analysis of microRNAs during the retinoic acid-induced neuronal differentiation of human NT2 cells, Nucleic Acids Res. Suppl. source
    • cites [131] Wang, 2010, Mouse microRNA-124 regulates the expression of Hes1 in P19 cells, Front. Biosci. source

      The Abstract reports that reducing miR-124 caused Hes-1 to accumulate and hindered retinoic-acid-induced neuronal differentiation in P19 cells. The claim instead names miR-23 and NT2 cells, neither of which is supported by that passage. (LLM, conf=0.88)

      Experimental — accuracy not yet measured

  • May combine two claims.

    Premisecitation

    The change of stress response mediated by miR-23 can be inherited and intervened by methyl modulator during lactation.

    “the change of stress response mediated by miR-23 can be inherited and intervened by methyl modulator during lactation.”
    Quote in the paperSubstantial claim1 of 2 sources checked
    • cites [126] Nemoto, 2023, Stress response abnormalities transgenerationally inherited via miR-23 downregulation are restored by a methyl modulator during the lactation period, J Dev Orig Health Dis source
    • cites [127] Fei, 2022, An integrated analysis of lactation-related miRNA and mRNA expression profiles in donkey mammary glands, Genes source

      The Results (§3.6) identify miR-23-3p as a potential regulator in lactating donkey mammary glands, and the Discussion (§4) links miR-23 to milk-lipid synthesis. Neither passage supports a miR-23-mediated change in stress response, inheritance of that change, or intervention with a methyl modulator. (LLM, conf=0.84)

      Experimental — accuracy not yet measured

  • May combine two claims.

    Premisecitation

    In rats with a fetal malnutrition model, expression of miR-23 was down-regulated in low birth weight rats, but the expression could be retrieved by methyl modulator after lactation.

    “In the rats with the fetal malnutrition model, it has been confirmed that the expression of miR-23 was down-regulated in the rats with low birth weight, but the expression could be retrieved by methyl modulator after lactation.”
    Quote in the paperNot a substantial claim1 of 2 sources checked
    • cites [126] Nemoto, 2023, Stress response abnormalities transgenerationally inherited via miR-23 downregulation are restored by a methyl modulator during the lactation period, J Dev Orig Health Dis source
    • cites [127] Fei, 2022, An integrated analysis of lactation-related miRNA and mRNA expression profiles in donkey mammary glands, Genes source

      The Discussion discusses miR-23 in donkey and goat mammary-gland biology, and Results §3.3 compares miRNA expression in lactating and nonlactating donkeys; neither addresses low-birth-weight rats. Searches for fetal malnutrition, miR-23 restoration, and methyl modulators found no passage supporting the claimed rat finding. The supplied copy gives no page numbers for these sections. (LLM, conf=0.78)

      Experimental — accuracy not yet measured

  • May combine two claims.

    Premisecitation

    Intervention with overexpression of miR-23a-3p can protect nerves and attenuate the apoptotic process and neuronal cell death.

    “intervention with overexpression of miR-23a-3p can protect nerves and attenuate the apoptotic process and neuronal cell death [139].”
    Quote in the paperSubstantial claim1 of 1 sources checked
    • cites [139] Sabirzhanov, 2020, Down-regulation of miR-23a-3p mediates irradiation-induced neuronal apoptosis, Int. J. Mol. Sci. source

  • May combine two claims.

    Premisecitation

    miR-23a-3p was found downregulated in mice cortex, hippocampus, and neurons after brain radiation, while the expression of Bcl family members was upregulated, causing secondary DNA damage.

    “The miR-23a-3p was found downregulated in mice cortex, hippocampus, and neurons after brain radiation, while the expression of Bcl family members was upregulated, causing secondary DNA damage.”
    Quote in the paperSubstantial claim1 of 1 sources checked
    • cites [139] Sabirzhanov, 2020, Down-regulation of miR-23a-3p mediates irradiation-induced neuronal apoptosis, Int. J. Mol. Sci. source

      Results §2.1 reports miR-23a-3p down-regulation in irradiated mouse cortex, hippocampus, and isolated neurons, alongside increased expression of selected pro-apoptotic Bcl-2 family members. The claim’s causal ending is not supported: the Discussion describes irradiation-induced DNA damage as preceding activation of p53 and up-regulation of those molecules, which then promote apoptosis—not as damage caused by their up-regulation. Bax was also not up-regulated in the cortex. (LLM, conf=0.89)

      Experimental — accuracy not yet measured

  • May combine two claims.

    Findingown data

    miR-23-3p has higher conservation among species, while miR-23-5p undergoes more nucleotide shifting.

    “The results displayed that miR-23–3p has higher conservation among species, while miR-23–5p undergoes more nucleotide shifting.”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Findingown data

    Sequence alignment revealed that miR-23b-5p is more conserved than miR-23a-5p, whereas miR-23b-3p is less conserved than miR-23a-3p.

    “Additionally, sequence alignment revealed that miR-23b-5p is more conserved than miR-23a-5p, whereas miR-23b-3p is less conserved than miR-23a-3p (Fig. 1E–H).”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisenone given

    In the human genome, the miR-23-27-24 cluster is composed of the miR-23a cluster (miR-23a-27a-24-2) and the miR-23b cluster (miR-23b-27b-24-1).

    “In the human genome, this cluster is composed of the miR-23a cluster (miR-23a–27a–24–2) and the miR-23b cluster (miR-23b–27b–24–1).”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Premisecitation

    Antagomirs can inhibit fibrosis development in newborn Alb/TGF-β1 transgenic mice, while injection in old mice restored existing fibrosis.

    “Antagomirs can inhibit fibrosis development in newborn Alb/TGF-β1 transgenic mice, while injection in old mice restored the existing fibrosis [17].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [17] Rogler, 2017, Knockdown of miR-23, miR-27, and miR-24 alters fetal liver development and blocks fibrosis in mice, Gene Expr. source

  • May combine two claims.

    Interpretationnone given

    miR-23 impacts the proliferation of liver cells and influences lipid metabolism in the liver.

    “Secondly, miR-23 not only impacts the proliferation of liver cells but also influences lipid metabolism in the liver.”
    Quote in the paperSubstantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisenone given

    The chromosomal locations of miR-23a and miR-23b differ across species; has-mir-23a/b are on human chromosomes 19 and 9, and mmu-mir-23a/b are on mouse chromosomes 8 and 13.

    “The has-mir-23a/b are located in chromosomes 19 and 9 of the human genome, respectively, whereas mmu-mir-23a/b are found on chromosomes 8 and 13 in the mouse genome, respectively.”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Premisecitation

    Direct injection of exogenous miR-23-27-24 cluster-specific inhibitor (antagomirs) into neonatal mice promoted bile duct differentiation and reduced hepatocyte proliferation.

    “direct injection of exogenous miR-23-27-24 cluster-specific inhibitor (named antagomirs) into neonatal mice promoted bile duct differentiation and reduced hepatocyte proliferation.”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [17] Rogler, 2017, Knockdown of miR-23, miR-27, and miR-24 alters fetal liver development and blocks fibrosis in mice, Gene Expr. source

  • May combine two claims.

    Premiseown data

    miR-23 is highly conserved across species and belongs to the miR-23-27-24 cluster but exists in different isoforms.

    “miR-23 is highly conserved across species and belongs to the miR-23-27-24 cluster but exists in different isoforms.”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisenone given

    miR-23 is subdivided into miR-23-3p and miR-23-5p.

    “Besides, miR-23 was further subdivided into miR-23–3p and miR-23–5p.”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Premisecitation

    Proteomics analysis indicates that miR-23 can enhance oxidative metabolism and mitochondrial activity through multiple targets, altering the balance of mammalian production cells and increasing productivity.

    “Proteomics analysis indicates that it can enhance oxidative metabolism and mitochondrial activity through multiple targets, thereby altering the balance of mammalian production cells and increasing productivity [24].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [24] Kelly, 2015, Re-programming CHO cell metabolism using miR-23 tips the balance towards a highly productive phenotype, Biotechnol. J. source

  • May combine two claims.

    Premisenone given

    Nucleotide shifting in miRNA genes can bring new functions or silence functions, resulting in loss-of-function and gain-of-function mutations.

    “The nucleotide shifting in miRNA genes can bring new functions or silence their functions, resulting in both loss-of-function mutations and gain-of-function mutations.”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Interpretationcitation

    miR-23 can serve as a biomarker for diagnosis of diabetes; measuring abnormal expression in plasma, liver, and adipose tissue can assess the development stage of diabetes.

    “Firstly, miR-23 can serve as a biomarker for the diagnosis of diabetes. By measuring the abnormal expression level of miR-23 in plasma, liver, and adipose tissue of patients, the development stage of diabetes can be assessed.”
    Quote in the paperSubstantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing), S4 (based). May combine two claims.

    Premisenone given

    miR-23a and miR-23b differ by only one nucleotide outside the seed sequence region but can display dissimilar functional roles when sharing identical target predictions.

    “Notably, despite only differing by one nucleotide outside the seed sequence region, miR-23a and miR-23b can still display dissimilar functional roles when sharing identical target predictions.”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Interpretationreasoning

    miR-23 is directly involved in the regulation of the development of many metabolic diseases such as liver fibrosis, obesity, and diabetes, and its expression level is commonly unusually up-regulated.

    “The aforementioned research has demonstrated that miR-23 is directly involved in the regulation of the development procedure of many metabolic diseases, such as liver fibrosis, obesity, and diabetes, and commonly, the expression level of miR-23 is unusually up-regulated.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Interpretationreasoning

    Differences in miR-23 isoform functions may be due to selective effects on their target proteins and differences in miRNA expression patterns.

    “This may be due to selective effects on their target proteins and differences in miRNA expression patterns, resulting in different functional types of miR-23 isoforms.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Premisecitation

    Normal expression of VEGF is crucial for maintaining the basic physiological state of retinal pigment epithelium tissue, and VEGF can be regulated by miR-23.

    “Therefore, the normal expression of vascular endothelium growth factor (VEGF) is crucial for maintaining the basic physiological state of this tissue, while current studies have shown that it can be regulated by miR-23.”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Premisecitation

    Reduction of miR-23 can inhibit VEGF expression and endothelial progenitor cell activity, and then restore blood flow in the ischemic limbs of mice.

    “The experiments performed in vivo also confirmed that the reduction of miR-23 can inhibit VEGF expression and endothelial progenitor cell activity, and then restore its blood flow in the ischemic limbs of mice [47].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [47] Di, 2015, miR-23 regulate the pathogenesis of patients with coronary artery disease, Int. J. Clin. Exp. Med.

      Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  • May combine two claims.

    Premisenone given

    More regulatory studies have focused on miR-23-3p, while miR-23-5p has only been specifically studied in liver fibrosis.

    “More regulatory studies have focused on miR-23–3p, while miR-23–5p has only been specifically studied in liver fibrosis (Table 1).”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Interpretationreasoning

    miR-23a has been popularly studied in immunity, serves as a marker of inflammation, and improves related diseases by varying its expression levels, rendering it a potential therapeutic target.

    “The above studies indicate that miR-23a has been popularly studied in immunity, and not only serve as a marker of inflammation but also improve related diseases by varying its expression levels, rendering it a potential therapeutic target.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Premisecitation

    The two isoforms of miR-23 can facilitate angiogenesis and influence endothelial cell apoptosis by directly targeting Sprouty2, but they have different effects on endothelial cell function.

    “Research has found that the two isoforms of miR-23 can facilitate angiogenesis and influence endothelial cell apoptosis by directly targeting Sprouty2 [42,43], but they have different effects on endothelial cell function.”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites [42] Zhou, 2011, Regulation of angiogenesis and choroidal neovascularization by members of microRNA-23∼27∼24 clusters, Proc. Natl. Acad. Sci. U. S. A. source
    • cites [43] Bang, 2012, Cardiovascular importance of the microRNA-23/27/24 family, Microcirculation source

  • May combine two claims.

    Premisecitation

    miR-23 is upregulated following phytosomal curcumin treatment and is involved in regulating PI3K/AKT1/NF-κB signaling pathways to enhance the immune modulation potential of human dental pulp stem cells.

    “Furthermore, miR-23 was found to be upregulated following phytosomal curcumin (PC) treatment and is involved in regulating PI3K/AKT1/NF-κB signaling pathways to enhance the immune modulation potential ability of Human dental pulp stem cells (hDPSCs) [33].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [33] Ayadilord, 2021, Immunomodulatory effects of phytosomal curcumin on related-micro RNAs, CD200 expression and inflammatory pathways in dental pulp stem cells, Cell Biochem. Funct. source

  • May combine two claims.

    Premisecitation

    miR-23a increases in mediating lysophosphatidic acid-induced cardiomyocyte hypertrophy, with LPA1 as the direct target, and miR-23a elevation can be restrained by PI3K inhibitors.

    “It was confirmed that miR-23a increased in mediating the lysophosphatidic acid (LPA) -induced cardiomyocyte hypertrophy, LPA1 was the direct target, however, miR-23a elevation can be restrained by PI3K inhibitors [52].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [52] Yang, 2013, Reciprocal regulation of miR-23a and lysophosphatidic acid receptor signaling in cardiomyocyte hypertrophy, Biochim. Biophys. Acta source

  • May combine two claims.

    Premisecitation

    In models of cardiac dysfunction, miR-23 can regulate cell metabolism and reduce injury through directly targeting GLS to restore glutamine metabolism and regulating CX43 to modulate mitochondrial autophagy.

    “In models of cardiac dysfunction, researchers have revealed that miR-23 can regulate cell metabolism and reduce injury through two pathways: directly targeting GLS to restore glutamine metabolism and regulating CX43 to modulate mitochondrial autophagy [53,54].”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites [53] Kou, 2016, Inhibition of miR-23 protects myocardial function from ischemia-reperfusion injury through restoration of glutamine metabolism, Eur. Rev. Med. Pharmacol. Sci.
    • cites [54] Wang, 2021, MiR-23a is involved in myocardial ischemia/reperfusion injury by directly targeting CX43 and regulating mitophagy, Inflammation source

  • May combine two claims.

    Premisecitation

    The miR-23-27-24 cluster regulates multiple dimensions of T cell biology and is an essential regulatory factor in T cell differentiation and function, playing a key role in controlling type II immunity.

    “The miR-23-27-24 cluster regulates multiple dimensions of T cell biology and is an essential regulatory factor in T cell differentiation and function, playing a key role in controlling type II immunity [26].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [26] Wu, 2015, miR-23∼27∼24 clusters restrict Th2 immunity and associated immunopathology during airway allergic reaction (HYP2P.335), J. Immunol. source

  • May combine two claims.

    Interpretationcitation

    miR-23 has been established as a biomarker and regulatory factor for inflammatory and autoimmune disorders such as rheumatoid arthritis.

    “Apart from directly regulating immune cells, miR-23 has also been established as a biomarker as well as a regulatory factor for inflammatory and autoimmune disorders, such as Rheumatoid arthritis (RA).”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Interpretationreasoning

    miR-23 is a regulatory factor tightly linked with cardiovascular disease, essential for maintaining the balance of the vascular system and regulating angiogenesis.

    “Previous studies have discovered that miR-23 is a regulatory factor tightly linked with cardiovascular disease, which is essential for maintaining the balance of the vascular system and regulating the process of angiogenic.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Interpretationreasoning

    miR-23a can serve as a reliable biomarker for detecting HCC and as a promising prognostic tool.

    “As a result, miR-23a can serve as a reliable biomarker for detecting HCC and making it a promising and reliable prognostic tool.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Premisecitation

    Up-regulated expression of miR-23a-3p has been identified in blood samples of acute cerebral hemorrhage patients and in a rat model of subarachnoid hemorrhage, leading to augmented apoptosis of cerebral vascular endothelial cells by suppressing ZO-1, and formation of cerebral hematoma.

    “Up-regulated expression of miR-23a-3p has been identified both in the blood samples of acute cerebral hemorrhage patients and in a rat model of subarachnoid hemorrhage, leading to augmented apoptosis of cerebral vascular endothelial cells by suppressing the expression of the target gene ZO-1, as well as the formation of cerebral hematoma.”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites [64] Hu, 2018, MicroRNA-23a-3p promotes the perihematomal edema formation after intracerebral hemorrhage via ZO-1, Eur. Rev. Med. Pharmacol. Sci. source
    • cites [65] Xue, 2022, Downregulation of miR-23a-3p improves cognitive function in rats after subarachnoid hemorrhage by targeting VCAN, Med. Mol. Morphol. source

  • May combine two claims.

    Premisecitation

    Acupuncture stimulation can down-regulate the expression of miR-23a-3p, thereby improving neurological dysfunction from intracerebral hemorrhage in rats, alleviating inflammation, ferroptosis, and neuronal cell death.

    “acupuncture stimulation can down-regulate the expression of miR-23a-3p, thereby improving the neurological dysfunction stemming from intracerebral hemorrhage (ICH) in rats, alleviating inflammation, ferroptosis, and neuronal cell death [67].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [67] Kong, 2021, Acupuncture ameliorates neuronal cell death, inflammation, and ferroptosis and downregulated miR-23a-3p after intracerebral hemorrhage in rats, J. Mol. Neurosci. source

  • May combine two claims.

    Premisecitation

    High expression of miR-23 can lead to a decrease in TASK-2 activity, and then increase the expression of acute regulatory proteins and aldosterone synthase in steroid production.

    “The high expression of miR-23 can lead to a decrease in TASK-2 activity, and then increase the expression of acute regulatory proteins and aldosterone synthase in steroid production [68].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [68] Lenzini, 2014, Lower expression of the TWIK-related acid-sensitive K+ channel 2 (TASK-2) gene is a hallmark of aldosterone-producing adenoma causing human primary aldosteronism, J. Clin. Endocrinol. Metab. source

  • May combine two claims.

    Premisecitation

    miR-23a-3p can promote the growth and metastasis of liver cancer cells and regulate chemotherapy sensitivity.

    “miR-23a-3p can promote the growth and metastasis of liver cancer cells and regulate chemotherapy sensitivity.”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [76] Xiang, 2020, MiR-23a-3p promoted G1/S cell cycle transition by targeting protocadherin17 in hepatocellular carcinoma, J. Physiol. Biochem. source

  • May combine two claims.

    Premisecitation

    Suppression of miR-23a-3p can inhibit apoptosis of cerebral microvascular endothelial cells by targeting VCAN, and promote cell activity and improve cognitive function after subarachnoid hemorrhage in rats.

    “Meanwhile, the suppression of miR-23a-3p can inhibit the apoptosis of cerebral microvascular endothelial cells by targeting VCAN, and thereafter promote cell activity and improve cognitive function after subarachnoid hemorrhage in rats [64,65].”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites [64] Hu, 2018, MicroRNA-23a-3p promotes the perihematomal edema formation after intracerebral hemorrhage via ZO-1, Eur. Rev. Med. Pharmacol. Sci. source
    • cites [65] Xue, 2022, Downregulation of miR-23a-3p improves cognitive function in rats after subarachnoid hemorrhage by targeting VCAN, Med. Mol. Morphol. source

  • May combine two claims.

    Premisecitation

    miR-23a-3p promotes tumor growth by reducing PCDH17, promoting transition of the HCC cell cycle.

    “miR-23a-3p promotes tumor growth by reducing the level of the target gene procalcadherin 17 (PCDH17), promoting the transition of the HCC cell cycle [76].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [76] Xiang, 2020, MiR-23a-3p promoted G1/S cell cycle transition by targeting protocadherin17 in hepatocellular carcinoma, J. Physiol. Biochem. source

  • May combine two claims.

    Interpretationreasoning

    Although abnormal expression of miR-23 in reproductive system-related cancers varies among different family members or displays cancers-independent patterns, they can all impact the development of cancer cells.

    “In general, although the abnormal expression of miR-23 in reproductive system-related cancers varies among different family members or displays cancers-independent, they can all impact on the development of cancer cells.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Premisecitation

    miR-23a expression level is elevated in postoperative glioma specimens of various grades, and this elevation is associated with downregulation of PTEN expression.

    “the expression level of miR-23a is elevated in postoperative glioma specimens of various grades, and this elevation is associated with the downregulation of PTEN expression”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [98] Koshkin, 2014, Analysis of expression of microRNAs and genes involved in the control of key signaling mechanisms that support or inhibit development of brain tumors of different grades, Clin. Chim. Acta source
    • cites [99] Xu, 2016, ATP5A1 and ATP5B are highly expressed in glioblastoma tumor cells and endothelial cells of microvascular proliferation, J. Neuro Oncol. source

  • May combine two claims.

    Premisecitation

    In glioblastoma microvascular proliferation tissue, miR-23 is downregulated, while its target genes ATP5A1 and ATP5B are highly expressed in endothelial cells.

    “In this context, miR-23 is downregulated, while its target genes ATP5A1 and ATP5B are highly expressed in endothelial cells.”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites [98] Koshkin, 2014, Analysis of expression of microRNAs and genes involved in the control of key signaling mechanisms that support or inhibit development of brain tumors of different grades, Clin. Chim. Acta source
    • cites [99] Xu, 2016, ATP5A1 and ATP5B are highly expressed in glioblastoma tumor cells and endothelial cells of microvascular proliferation, J. Neuro Oncol. source

  • May combine two claims.

    Premisecitation

    miR-23 is among differentially expressed miRNAs within 89 children cases with acute lymphoblastic leukemia by high throughput sequencing, and BCL2 was its anti-apoptotic target.

    “miR-23 is among the differentially expressed miRNAs within 89 children cases with acute lymphoblastic leukemia (ALL) by high throughput sequencing, and B-cell lymphoma 2 (BCL2) was its anti-apoptotic target [93].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [93] Schotte, 2011, Discovery of new microRNAs by small RNAome deep sequencing in childhood acute lymphoblastic leukemia, Leukemia source

  • May combine two claims.

    Interpretationreasoning

    miR-23a/b can exhibit different expression patterns, such as in ovarian cancer, or display a similar regulation role in thymic lymphoma.

    “miR-23a/b can exhibit different expression patterns, such as in OC, or display a similar regulation role in thymic lymphoma.”
    Quote in the paperSubstantial claim

  • Probably not a substantial claim: may not pass S2 (checkable). May combine two claims.

    Interpretationreasoning

    These studies provide a comprehensive generality of the complex regulatory networks involving miR-23a and miR-23b in tumor biology, emphasizing their potential as therapeutic targets for cancer treatment.

    “these studies provide a comprehensive generality of the complex regulatory networks involving miR-23a and miR-23b in tumor biology, emphasizing their potential as therapeutic targets for cancer treatment (Fig. 4).”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Interpretationcitation

    Under normal physiological conditions of bone, miR-23 can maintain a stable low expression level, which is more beneficial for its growth and development.

    “This indicates that under normal physiological conditions of bone, miR-23 can maintain a stable low expression level, which is more beneficial for its growth and development.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Interpretationcitation

    miR-23 needs to be maintained at a certain expression level during the growth and development of organ tissues, and the lack of it may affect cell regeneration.

    “miR-23 needs to be maintained at a certain expression level during the growth and development of organ tissues, and the lack of it may affect cell regeneration.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Premisereasoning

    Overexpression of miR-23-3p is advantageous to endometrial receptivity and embryo implantation, enhancing the adhesion ability of trophoblast spheroids for normal conception.

    “overexpression of miR-23–3p is advantageous to endometrial receptivity and embryo implantation, enhancing the adhesion ability of trophoblast spheroids for normal conception.”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites [4] Barton, 2023, miR-23b-3p regulates human endometrial epithelial cell adhesion implying a role in implantation, Reproduction source
    • cites [125] Huang, 2020, miR-23a-3p increases endometrial receptivity via CUL3 during embryo implantation, J. Mol. Endocrinol. source

  • May combine two claims.

    Premisecitation

    Expression of miR-23-3p is upregulated in endometrial epithelial cells of pregnant mice, and its expression level is positively correlated with pregnancy time.

    “The expression of miR-23–3p is upregulated in endometrial epithelial cells of pregnant mice, and its expression level is positively correlated with pregnancy time.”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [4] Barton, 2023, miR-23b-3p regulates human endometrial epithelial cell adhesion implying a role in implantation, Reproduction source
    • cites [125] Huang, 2020, miR-23a-3p increases endometrial receptivity via CUL3 during embryo implantation, J. Mol. Endocrinol. source

  • May combine two claims.

    Interpretationcitation

    Although overexpression of miR-23 can promote apoptosis, it can also promote embryo implantation in reproductive progress, exhibiting a positive effect.

    “Although overexpression of miR-23 can promote apoptosis, it can also promote embryo implantation in the reproductive progress, exhibiting a positive effect.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Interpretationreasoning

    Different isoforms of miR-23 can target common target genes, yet their functions can vary.

    “Thirdly, different isoforms of miR-23 can target common target genes, yet their functions can vary.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Premisereasoning

    miR-23 participates in regulating macrophages during inflammation, tumor cell proliferation, and heart cell development.

    “participate in regulating macrophages during inflammation (Fig. 2), tumor cell proliferation (Fig. 4), and heart cell development (Fig. 5).”
    Quote in the paperSubstantial claim

  • Probably not a substantial claim: may not pass S4 (based).

    Premisenone given

    miR-23 can interact with the sequence of lncRNA Malat1.

    “miR-23 can interact with the sequence of lncRNA Malat1”
    Quote in the paperNot a substantial claim

  • The quote only partly states this claim.

    Interpretationreasoning

    Research findings reveal a favorable therapeutic effect of intervening with inhibitors or overexpression of miR-23.

    “the research findings also reveal a favorable therapeutic effect.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Interpretationcitation

    miR-23a-3p suppression in epilepsy can reduce brain damage, while its overexpression after brain radiation reduces neuronal apoptosis.

    “miR-23a-3p suppression in epilepsy can reduce brain damage, while its overexpression after brain radiation reduces neuronal apoptosis.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Interpretationreasoning

    miR-23 may have diverse regulatory functions through its fixed combination, making it a central regulatory hub for these processes.

    “This suggests that miR-23 may have diverse regulatory functions through its fixed combination, making it a central regulatory hub for these processes.”
    Quote in the paperSubstantial claim

  • Probably not a substantial claim: may not pass S4 (based). May combine two claims.

    Premisenone given

    Existing studies indicate that miR-23 demonstrates a certain expression in different tissues, which can be detected, and diseased tissues can also have an impact on their expression level.

    “Existing studies have indicated that miR-23 demonstrates a certain expression in different tissues, which can be detected, and diseased tissues can also have an impact on their expression level.”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing), S4 (based).

    Interpretationnone given

    The miR-23 family is capable of exerting a regulatory influence on organisms independently, either as a functional cluster or as a solitary regulator.

    “is capable of exerting a regulatory influence on organisms independently, either as a functional cluster or as a solitary regulator.”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing), S4 (based).

    Interpretationnone given

    The miR-23 family is immensely conserved amidst diverse species.

    “The miR-23 family is immensely conserved amidst diverse species”
    Quote in the paperNot a substantial claim
112 of 112

  • The paper relies on this without support.

    The untapped effects of miR-23 on organisms, whether as a functional cluster or a single regulator, have not been systematically elucidated.

    “Furthermore, the untapped effects of miR-23 on organisms, whether as a functional cluster or a single regulator, has not been systematically elucidated yet.”
1 of 1

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

Each contradiction between two passages listed here was confirmed by an independent check.

  • Opposite miR-23 expression directions reported for metabolic syndrome

    Major

    The text says miR-23-3p is upregulated in metabolic syndrome, but Table 1 lists miR-23a-3p as downregulated in metabolic syndrome.

  • Melanoma proliferation claim reverses the cited reference's direction

    Minor

    The text says that lowering Malat1 raises miR-23a and consequently promotes tumor-cell proliferation. The cited melanoma reference instead says MALAT1 promotes proliferation by downregulating miR-23a.

2 of 2

Cited works that were retracted

Works this paper cites that were later retracted, from the retraction notices publishers deposit. Major when the notice came out before this paper was published.

  • Cites a retracted work: 10.1002/jcb.20982

    Info

    The cited work was retracted on 2025-04-28 (notice 10.1002/jcb.70023), not before this paper was published (2025-04).

    Cited work 10.1002/jcb.20982 · retracted 2025-04-28 · notice 10.1002/jcb.70023 · this paper published 2025-04

1 of 1

Cites

1 retracted

Flagged first, then by citations

8 of the 148 references couldn’t be matched to a known paper.

Cited by

Sorted by citations

Related

Authors
Qian, X., Jiang, Y., Yang, Y., Zhang, Y., Xu, N., Xu, B., Pei, K., Yu, Z., & Wu, W.
Affiliations
  • Nanjing University of Chinese Medicine (CN)
  • Capital Medical University (CN)
Corresponding author
  • Pei, Ke
  • Yu, Zhi
  • Wu, Wei
ORCID
Venue
Non-coding RNA Research
Publisher
Elsevier BV
Published
2025-04
Volume
11
Pages
220-233
ISSN
2468-0540 (ISSN-L)
DOI
10.1016/j.ncrna.2024.12.010
PMC
PMC11787465
OpenAlex
W4405910171
Semantic Scholar
29c7dd21fc246d95a836c44fb33b486ba84b5ad3
Cited by
5
References
148
Citations by year
2026: 4 · 2025: 1
FWCI
0.76
Type
journal article
Language
en
Open access
Licence
Locations
  • Non-coding RNA Research (publishedVersion, cc-by-nc-nd)
  • PubMed (publishedVersion)
  • PubMed Central (submittedVersion, cc-by-nc-nd)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
National Natural Science Foundation of China (81873238, 82374577)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
  • Life Sciences › Agricultural and Biological Sciences › Plant Science › Plant Molecular Biology Research
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer-related molecular mechanisms research
Keywords
miR-23, microRNA isoforms, miRNA families, microRNA binding sites, metabolic disorders, immune response, cardiovascular disease, cancer, organogenesis, nervous system function, disease biomarkers

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Claims read by deepseek-v4.1-flash under definition version 3 (extract-v3) on 2026-10-20.

Classified by jev-1.13-20260917 (gold-guideline-v0.2) on 2026-10-20.

Cited sources are checked by gpt-6-sol.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

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