ArticleJournal of musculoskeletal & neuronal interactions2025
ALKBH5 Regulates Apoptosis of Rheumatoid Arthritis Fibroblast-like Synoviocytes by Modulating miR-181b-5p Maturation via m6A Demethylation.
Article in Journal of musculoskeletal & neuronal interactions, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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Who cites it
4 citing papers in PubMed.
- Clerodendrum japonicum Extract Suppresses the Pathogenicity of Rheumatoid Arthritis Fibroblast-Like Synoviocytes by Inhibiting METTL3-Mediated ICAM2 mRNA Methylation.Cell biochemistry and function · 2026Article
- METTL3-Mediated m6A Regulation of CircINTS4/miR-146b-3p Axis in Rheumatoid Arthritis.Inflammation · 2026Article
- Metabolic control of RNA methylation in rheumatoid arthritis: from synovial stress to pathogenic cellular adaptation.Frontiers in immunology · 2026Review
- The PANoptotic mosaic of rheumatoid arthritis: epitranscriptomic regulation, systemic relays, and precision death-mode editing.Frontiers in immunology · 2026Review
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo investigate the role of ALKBH5, a member of the AlkB family of Fe(II)/α-KG-dependent dioxygenases that functions as an RNA demethylase removing N6-methyladenosine (m6A), in regulating apoptosis of rheumatoid arthritis fibroblast-like synoviocytes (RA-FLS), with a focus on miR-181b-5p maturation.
methodsRA-FLS were isolated and analyzed for ALKBH5, pre-miR-181b-1, and miR-181b-5p expression using qRT-PCR. ALKBH5 protein levels were assessed by Western blotting. Cell proliferation and apoptosis were evaluated using MTT assay and flow cytometry, respectively. m6A modification on pre-miR-181b-1 was measured via MeRIP, and its binding to DGCR8 was assessed using co-immunoprecipitation.
resultsALKBH5 expression was significantly downregulated in RA-FLS. ALKBH5 overexpression inhibited proliferation and promoted apoptosis, while its knockdown had the opposite effect. ALKBH5 decreased m6A modification of pre-miR-181b-1, thereby increasing levels of pre-miR-181b-1 and mature miR-181b-5p. Inhibition of miR-181b-5p attenuated the effects of ALKBH5.
conclusionOverexpression of ALKBH5 promotes apoptosis and inhibits proliferation in RA-FLS by demethylating m6A on pre-miR-181b-1, thereby enhancing miR-181b-5p maturation. These findings suggest a novel therapeutic target for rheumatoid arthritis.
Indexed as
Identifiers
41324215PMC12684260What OpenQuestion holds
Registered trials
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