Dysregulation of Different Modes of Programmed Cell Death in Rheumatoid Arthritis Fibroblast‐Like Synoviocyte

Rheumatoid arthritis (RA) is a chronic inflammatory disease characterized by chronic synovitis and skeletal joint deformities, often accompanied by systemic symptoms. Over the past few decades, various susceptibility factors for RA have been revealed, and numerous therapeutic drugs have been developed, including analgesics, glucocorticoids, non-steroidal anti-inflammatory drugs (NSAIDs), disease-modifying antirheumatic drugs (DMARDs), and biological agents (bDMARDs). Despite the availability of multiple treatment options, the therapeutic outcomes for some patients remain suboptimal due to the complex pathogenesis of RA. As a key pathological mechanism, programmed cell death (PCD) in RA has received extensive attention. Dysregulation of PCD in RA impacts the progression of the disease. This article systematically reviews the roles of various cell death modalities, including apoptosis, necroptosis, ferroptosis, pyroptosis, and autophagy in the pathophysiology of RA, aiming to provide a theoretical basis and direction for the discovery of new therapeutic targets and drug development.