ArticleFrontiers in immunology2024
YTHDC1 Regulates the Migration, Invasion, Proliferation, and Apoptosis of Rheumatoid Fibroblast-Like Synoviocytes.
Article in Frontiers in immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Integrative Network Toxicology, Machine Learning, Single-Cell Analysis, scTenifoldKnk-Based Virtual Knockout, and Molecular Docking Suggest a Potential Molecular Link Between Aspartame and Rheumatoid Arthritis InvolvingInternational journal of molecular sciences · 2026Article
- TAF1 aggravates ferroptosis by promoting the ubiquitin-mediated degradation of nuclear GPX4.Journal of Zhejiang University. Science. B · 2026Article
- METTL3-Mediated m6A Regulation of CircINTS4/miR-146b-3p Axis in Rheumatoid Arthritis.Inflammation · 2026Article
- Immunometabolic reprogramming in rheumatoid arthritis: the epitranscriptomic role of N6-methyladenosine in innate and adaptive immunity.Frontiers in immunology · 2026Review
- Unveiling potential diagnostic biomarkers for rheumatoid arthritis through integrated gene expression analysis.Frontiers in immunology · 2026Article
- RNA methylation in autoimmune rheumatic diseases: mechanisms and therapeutic potential.Frontiers in immunology · 2026Review
- Epigenetic modifier m⁶A methylation: insights into the pathogenesis and therapeutic potential of autoimmune diseases.Journal of translational medicine · 2025Review
- Regulatory roles of 13 types of RNA modifications in osteoarthritis: based on bulk and single-cell RNA analysis.3 Biotech · 2025Article
- The Role and Mechanism of Protein Post‑Translational Modification in Rheumatoid Arthritis.Journal of inflammation research · 2025Review
- Exosome circ-CBLB promotes M1 macrophage polarization in rheumatoid arthritis through the TLR3/TRAF3 signaling axis.Frontiers in immunology · 2025Article
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9 authors.
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Abstract
Background: Rheumatoid arthritis (RA), a chronic autoimmune condition, is characterized by persistent synovial inflammation, bone degradation, and progressive joint deterioration. Despite considerable research efforts, the precise molecular mechanism underlying RA remains elusive. This investigation aims to elucidate the potential role and molecular mechanism of N6-methyladenosine (m Methods: In this study, we employed bioinformatics tools to elucidate the association between RA and m Results: Differential expression analysis, PPI analysis, and single-cell analysis identified three key hub genes (YTHDC1, YTHDC2, and YTHDF2) associated with RA. GSEA results further revealed that these genes are enriched in pathways associated with inflammatory responses. Subsequent correlation analysis demonstrated a significant negative correlation between YTHDC1 expression and CD8+ T cell levels. Notably, the gene and protein expression levels of YTHDC1 and YTHDF2 were significantly reduced in the synovial tissue of RA patients. Furthermore, silencing YTHDC1 in fibroblast-like synoviocytes (FLSs) significantly inhibited their migration, invasion, proliferation, and induced apoptosis. Conclusion: YTHDC1 may potentially be involved in the pathogenesis of RA through its regulation of migration, invasion, proliferation, and apoptosis in FLSs.
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