The miR-23–27–24 cluster: an emerging target in NAFLD pathogenesis
Open accessAbstract
The incidence of non-alcoholic fatty liver disease (NAFLD) is increasing globally, being the most widespread form of chronic liver disease in the west. NAFLD includes a variety of disease states, the mildest being non-alcoholic fatty liver that gradually progresses to non-alcoholic steatohepatitis, fibrosis, cirrhosis, and eventually hepatocellular carcinoma. Small non-coding single-stranded microRNAs (miRNAs) regulate gene expression at the miRNA or translational level. Numerous miRNAs have been shown to promote NAFLD pathogenesis and progression through increasing lipid accumulation, oxidative stress, mitochondrial damage, and inflammation. The miR-23-27-24 clusters, composed of miR-23a-27a-24-2 and miR-23b-27b-24-1, have been implicated in various biological processes as well as many diseases. Herein, we review the current knowledge on miR-27, miR-24, and miR-23 in NAFLD pathogenesis and discuss their potential significance in NAFLD diagnosis and therapy.
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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.”
From Recent advances of miR-23 in human diseases and growth development (2025) · cites this paper as [9]
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)
Experimental — accuracy not yet measuredIn vivo and in vitro experiments indicated that miR-23a-3p can combine with PGC-1α to advance lipid metabolism and lessen alcoholic liver injury.
“In vivo and in vitro experiments have indicated that it can combine with peroxisome proliferator activated receptor-gamma coactivator 1-alpha (PGC -1α) to advance lipid metabolism and lessen alcoholic liver injury [9,19].”
From Recent advances of miR-23 in human diseases and growth development (2025) · cites this paper as [9]
The ‘MIR-24 AND MIR-23’ section links miR-23a to PGC-1α, but reports that downregulating miR-23a increased PGC-1α expression and reduced HepG2 cell apoptosis. It also reports that attenuating miR-23a alleviated hepatic steatosis. These passages do not establish that miR-23a-3p binds PGC-1α to improve lipid metabolism or lessen alcoholic liver injury, nor do they describe both in vivo and in vitro experiments for that claim. (LLM, conf=0.84)
Experimental — accuracy not yet measuredmiR-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.”
From Recent advances of miR-23 in human diseases and growth development (2025) · cites this paper as [9]
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)
Experimental — accuracy not yet measured
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Cited by
Sorted by citations
Recent advances of miR-23 in human diseases and growth development
Qian, X., Jiang, Y., Yang, Y., Zhang, Y., Xu, N., Xu, B., Pei, K., Yu, Z., & Wu, W. (2025) · Non-coding RNA Research · doi:10.1016/j.ncrna.2024.12.010 · Cited by 5 · see citing works
- Authors
- Ru, L., Wang, X.-M., & Niu, J.-Q.
- Affiliations
- First Hospital of Jilin University (CN)
- Venue
- Acta Pharmacologica Sinica
- Published
- 2021-12-10
- Volume
- 43
- Issue
- 5
- Pages
- 1167-1179
- ISSN
- 0253-9756 (ISSN-L)
- 1671-4083
- 1745-7254
- PMC
- PMC9061717
- OpenAlex
- W4200343858
- Cited by
- 21
- References
- 8
- Citations by year
- 2026: 5 · 2025: 2 · 2024: 9 · 2023: 2 · 2022: 3
- FWCI
- 0.42
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Acta Pharmacologica Sinica (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Natural Science Foundation of Jilin Province (20210101446JC)
- National Natural Science Foundation of China (81970519, 2017TD-08)
- People's Government of Jilin Province
- Fundamental Research Funds for the Central Universities (2017TD-08)
- Program for Jilin University Science and Technology Innovative Research Team (2017TD-08)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
- Health Sciences › Medicine › Epidemiology › Liver Disease Diagnosis and Treatment
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Keywords
- microRNA, non-alcoholic fatty liver disease, miR-27, miR-24, miR-23, lipid accumulation, oxidative stress, mitochondrial damage, inflammation, NAFLD diagnosis, NAFLD therapy
- MeSH terms
- Carcinoma, Hepatocellular, Humans, Liver, Liver Cirrhosis, Liver Neoplasms, MicroRNAs, Non-alcoholic Fatty Liver Disease
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