microRNA‑23 inhibits inflammation to alleviate rheumatoid arthritis via regulating CXCL12
Open accessAbstract
Rheumatoid arthritis (RA) is a common systemic, inflammatory and autoimmune disorder. MicroRNAs (miRs) are strongly associated with the initiation and progression of RA. However, the functions and mechanisms underlying miR-23 in RA are not completely understood. Therefore, the present study aimed to investigate the molecular mechanisms underlying miR-23 in RA. A bioinformatics tool (StarBase) and a wide range of experimental assays, including reverse transcription-quantitative PCR, western blotting, luciferase reporter assays and ELISAs, were performed to investigate the biological role of miR-23 in RA. The results indicated that miR-23 was downregulated and chemokine C-X-C motif ligand 12 (CXCL12) was upregulated in RA samples compared with healthy samples. Furthermore, miR-23 overexpression suppressed inflammation via reducing TNF-α, IL-1β and IL-8 expression levels compared with the NC mimic group. Regarding the underlying mechanism, compared with NC mimic, miR-23 mimic decreased CXCL12 mRNA expression by binding to its 3'-untranslated region. Additionally, CXCL12 overexpression reversed miR-23 mimic-mediated effects on inflammation. NF-κB signaling is associated with inflammation. Therefore, the present study indicated that CXCL12 promoted inflammation by activating NF-κB signaling. In conclusion, miR-23 inhibited inflammation to alleviate RA by regulating CXCL12 via the NF-κB signaling pathway, which may serve as a potential target for the diagnosis and treatment of RA.
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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.”
From Recent advances of miR-23 in human diseases and growth development (2025) · cites this paper as [31]
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)
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Experimental — accuracy not yet measuredExpression 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.”
From Recent advances of miR-23 in human diseases and growth development (2025) · cites this paper as [31]
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 measuredOverexpression of CXCL12 activates the NF-κB signaling pathway to promote inflammation.
“Overexpression of CXCL12 activates the NF-κB signaling pathway to promote inflammation [13,31].”
From Recent advances of miR-23 in human diseases and growth development (2025) · cites this paper as [31]
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References 44 · Cited by 12
- Authors
- Gao, B., Sun, G., Wang, Y., Geng, Y., Zhou, L., & Chen, X.
- Affiliations
- Nanjing Medical University (CN)
- Corresponding author
- Zhou, Lei
- Venue
- Experimental and Therapeutic Medicine
- Publisher
- Spandidos Publications
- Published
- 2021-03-03
- Volume
- 21
- Issue
- 5
- Pages
- 459-459
- ISSN
- 1792-0981 (ISSN-L)
- 1792-1015
- PMC
- PMC7967800
- OpenAlex
- W3133860565
- Cited by
- 12
- References
- 44
- Citations by year
- 2025: 5 · 2024: 3 · 2023: 1 · 2022: 3
- FWCI
- 1.32
- Type
- journal article
- Language
- en
- Open access
- diamond
- doi.org
- Licence
- cc-by-nc-nd
- Locations
- Experimental and Therapeutic Medicine (publishedVersion, cc-by-nc-nd)
- PubMed Central (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Rheumatology › Rheumatoid Arthritis Research and Therapies
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
- Health Sciences › Medicine › Complementary and alternative medicine › Natural Compounds in Disease Treatment
- Keywords
- rheumatoid arthritis, CXCL12, inflammation, NF-κB signaling, 3' untranslated region, TNF-α, IL-1β, interleukin-8, chemokines, microRNA therapeutic target
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