Narrative review demonstrates that dysregulated programmed cell death drives joint destruction in rheumatoid arthritis, highlighting potential therapeutic targets for clinical care.
Rheumatoid arthritis (RA) is a chronic, progressive, systemic autoimmune disease characterised by synovial inflammation, synovial pannus formation and subsequent destruction of articular cartilage and bone. Programmed cell death (PCD), encompassing apoptosis, autophagy, pyroptosis, necroptosis, and ferroptosis, plays a pivotal role in the pathogenesis of RA. An imbalance in PCD causes a variety of immune cells to release large amounts of inflammatory factors and mediators that exacerbate not only chronic synovial inflammation, but also bone and joint damage. The purpose of this article is to review the relevant studies between PCD and RA, with the aim of providing further insights and considerations for a deeper understanding of the pathogenesis of RA and to guide clinical management.
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Tong et al. (2025) studied this question.
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