The Role of Synovitis and Latent Transcription Factors in the Pathogenesis of Rheumatoid Arthritis

Rheumatoid Arthritis (RA) is a chronic autoimmune inflammatory disease that affects synovial membranes, leading to relentless progressive joint damage. This pathological process is regulated by transcription factors, such as NF-κB, STAT3, TGF-β, WNT, p38 MAPK, mTOR, AP-1, TLR-4, SOCS-4, YY-1, IRF, and FGF-20, which enhance the production of matrix-degrading enzymes and proinflammatory cytokines. Dysregulation of these transcription factors amplifies inflammation and accelerates joint damage, making them potential therapeutic targets.

The purpose of this review was to summarize the role of transcription factors in RA and the onset of synovitis and identify potential therapeutic targets to mitigate joint damage.

A comprehensive search of electronic databases (PubMed, Google Scholar, and Web of Science) was conducted. Additionally, searches of government health ministries and websites were performed to retrieve relevant information. Records available until March 12, 2024, were considered. Screening (primary and secondary) of the records and data extraction from eligible studies were carried out.

Synovitis sustains a proinflammatory environment mediated by dysregulated transcription factors, as mentioned earlier. These transcription factors promote the production of inflammatory cytokines and matrix-degrading enzymes, leading to progressive joint destruction. Therefore, targeting these transcription factors or their upstream regulators may offer promising therapeutic interventions for RA.

The pathogenesis of RA centers on transcription factors responsible for the inflammatory and destructive processes in synovitis. These molecules are ideal targets for developing novel treatments. Further elucidation of their complex molecular interactions and advancements in personalized therapies for RA patients is necessary.