{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,17]],"date-time":"2026-07-17T06:10:23Z","timestamp":1784268623777,"version":"3.55.0"},"reference-count":82,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,7,17]],"date-time":"2026-07-17T00:00:00Z","timestamp":1784246400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:p>Rheumatoid arthritis (RA) is a chronic autoimmune disorder characterized by persistent synovitis, invasive pannus formation, cartilage degradation, and bone erosion. Although metabolic reprogramming and epigenetic dysregulation are increasingly recognized as central features of rheumatoid arthritis, the mechanisms by which local metabolic stress is converted into durable pathogenic cellular states remain incompletely understood. Recent advances in epitranscriptomics suggest that dynamic RNA modifications, particularly RNA methylation, act as critical post-transcriptional regulators of immune and stromal cell adaptation. Local hypoxia, enhanced glycolytic flux, lactate accumulation, mitochondrial dysfunction, oxidative stress, and lipid metabolic imbalance collectively influence the expression, activity, substrate availability, and transcript selectivity of RNA methylation regulators. These metabolically conditioned RNA modification programs, including canonical N6-methyladenosine (m6A) and emerging non-m6A marks such as internal N7-methylguanosine (m7G), may help stabilize pathogenic phenotypes across multiple cell types. In fibroblast-like synoviocytes (FLS), RNA methylation sustains glycolytic fitness, invasive behavior, and resistance to apoptosis and ferroptosis. In macrophages, it reinforces inflammatory polarization and extracellular vesicle-mediated communication. In T cells and neutrophils, it contributes to Th17 skewing, defective autophagy, oxidative stress responses, and excessive neutrophil extracellular trap (NET) formation. We further discuss how RNA methylation integrates non-coding RNA networks, extracellular vesicle signaling, and regulated cell death pathways to maintain chronic synovial inflammation and tissue destruction. Finally, we highlight the translational implications of this metabolic\u2013epitranscriptomic interface, including biomarker discovery, patient stratification, and microenvironment-informed therapeutic strategies. Targeting both metabolic stress and RNA methylation-dependent adaptation may provide new opportunities for precision-oriented intervention in rheumatoid arthritis.<\/jats:p>","DOI":"10.3389\/fimmu.2026.1865927","type":"journal-article","created":{"date-parts":[[2026,7,17]],"date-time":"2026-07-17T05:44:05Z","timestamp":1784267045000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Metabolic control of RNA methylation in rheumatoid arthritis: from synovial stress to pathogenic cellular adaptation"],"prefix":"10.3389","volume":"17","author":[{"given":"Shu","family":"Li","sequence":"first","affiliation":[{"name":"The First Affiliated Hospital of Anhui University of Chinese Medicine","place":["Hefei, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lei","family":"Wan","sequence":"additional","affiliation":[{"name":"The First Affiliated Hospital of Anhui University of Chinese 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