Abstract
Rheumatoid arthritis (RA) is a chronic inflammatory joint disease that can lead to clinical manifestations of systemic diseases. Its leading features include chronic synovial inflammation and degeneration of the bones and joints. In the past decades, multiple susceptibilities for rheumatoid arthritis have been identified along with the development of a remarkable variety of drugs for its treatment; which include analgesics, glucocorticoids, nonsteroidal anti-inflammatory medications (NSAIDs), disease-modifying anti-rheumatic drugs (DMARDs), and biologic response modifiers (bDMARDs). Despite the existence of many clinical treatment options, the prognosis of some patients remains poor due to complex mechanism of the disease. Programmed cell death (PCD) has been extensively studied and ascertained to be one of the essential pathological mechanisms of RA. Its dysregulation in various associated cell types contributes to the development of RA. In this review, we summarize the role of apoptosis, cell death-associated neutrophil extracellular trap formation, necroptosis, pyroptosis, and autophagy in the pathophysiology of RA to provide a theoretical reference and insightful direction to the discovery and development of novel therapeutic targets for RA.
Highlights
Rheumatoid arthritis (RA) is an autoimmune disease that is usually accompanied by swelling, tenderness, and pain in the joints
Several studies have shown that the imbalance of Programmed cell death (PCD) in promoting the chronic inflammation of the synovial membrane, joint erosion, and destruction, as well as angiogenesis plays an important role in promoting RA
We have deliberated over the irregular apoptotic pattern of autoimmune T cells, B cells, inflammatory monocytes, inflammatory macrophages, and osteoclasts, which results in prolonged cell survival, thereby facilitating continuous presentation of autoantigens, the release of inflammatory factors, and the destruction of bones and joints
Summary
RA is an autoimmune disease that is usually accompanied by swelling, tenderness, and pain in the joints. Programmed Cell Death in RA synovial membrane and destruction of bones and joints during RA progression. These effects characterize the immune disorder of RA, which involves immune complex-mediated complement activation, immune response to the posttranslationally modified protein autoantigen, dysregulation of cell factor network, and activation of bone destruction-related cells [3,4,5]. At present, targeted immunotherapy with specific mechanisms (biologically targeted agents and various kinase inhibitors) has made significant progress in the clinical treatment of RA, thereby significantly improving the clinical outcomes in patients These therapies have been demonstrated to target key molecules and cell nodes that are enriched in the complex mechanism of the disease. This review aims to describe the various forms of PCD that may play critical role in the progression of RA, thereby providing insightful reference and direction for further analysis of disease mechanisms and targeted development of innovative therapies for clinical use
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