Abstract

Rheumatoid arthritis (RA) is a progressive autoimmune disease characterized by chronic synovitis and articular destruction. Pain is the earliest and most important symptom. The Janus kinase/stat signaling pathway not only participates in the physiological processes such as the growth and differentiation of normal cells, but also plays a significant role in the pathological mechanisms such as pain in RA patients. Pain in RA patients is mediated by both inflammatory and non-inflammatory factors, including central sensitization and peripheral sensitization. Cytokines can regulate the nociceptor threshold through the JAK pathway, which leads to sensitization. In this review, we provide an overview of the physiological basis of pain modulation, the underlying importance of cytokines and JAK/STAT pathway in pain modulation, and finally introduce the performance of JAK inhibitors in clinical research. Having a better understanding of the mechanism of pain in RA may provide new therapeutic ideas and directions for the clinical improvement of pain in RA patients.

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