凋亡是一个复杂的调节性、主动的细胞死亡过程，在细胞发育、稳态和衰老中发挥作用。癌症、发育缺陷和退行性疾病都是由于凋亡失调引起的病理性疾病。而骨关节炎（OA）是老年人中最常见的关节疾病，其特点是关节软骨的持续破坏，导致严重的残疾。多种变量调节软骨基质的合成和降解途径，这些变量直接或间接地促进了骨关节炎中软骨退变的发生。关节软骨是一种高度特化的组织，由紧密排列在一起的细胞外基质组成。因此，软骨细胞的存活对于保持理想的软骨基质至关重要，软骨细胞的特征和存活损害可能导致关节软骨衰竭。炎症细胞因子可以促进或抑制程序性细胞死亡的过程。如TNF-α等亲凋亡细胞因子可以诱导细胞死亡，而IL-4和IL-10等抗凋亡细胞因子可以保护细胞免受凋亡的影响。这些细胞因子之间的平衡在决定细胞命运方面起着关键作用，并对组织损伤和疾病进展产生影响。同样地，它们通过促进降解和合成途径破坏关节组织的代谢平衡，从而促进骨关节炎的发展。细胞关节的作用以及细胞信号通路对细胞因子和炎症物质的影响，决定了它们在骨关节炎发展中的功能。虽然凋亡在骨关节炎软骨中明显存在，但是确定凋亡性软骨细胞在骨关节炎发病机制中的相对作用是困难的，并且凋亡性软骨细胞的比率在骨关节炎软骨中并不一致。本研究总结了凋亡在骨关节炎发展中的作用、触发事件级联反应的介质和信号通路以及其他炎症特征。版权所有© Bentham Science Publishers；有关任何疑问，请发送电子邮件至epub@benthamscience.net。

Apoptosis is a complex regulatory, active cell death process that plays a role in cell development, homeostasis, and ageing. Cancer, developmental defects, and degenerative diseases are all pathogenic disorders caused by apoptosis dysregulation. Osteoarthritis (OA) is by far the most frequently diagnosed joint disease in the aged, and it is characterized by the ongoing breakdown of articular cartilage, which causes severe disability. Multiple variables regulate the anabolic and catabolic pathways of the cartilage matrix, which either directly or indirectly contribute to cartilage degeneration in osteoarthritis. Articular cartilage is a highly specialized tissue made up of an extracellular matrix of cells that are tightly packed together. As a result, chondrocyte survival is crucial for the preservation of an optimal cartilage matrix, and chondrocyte characteristics and survival compromise may result in articular cartilage failure. Inflammatory cytokines can either promote or inhibit apoptosis, the process of programmed cell death. Pro-apoptotic cytokines like TNF-α can induce cell death, while anti-apoptotic cytokines like IL-4 and IL-10 protect against apoptosis. The balance between these cytokines plays a critical role in determining cell fate and has implications for tissue damage and disease progression. Similarly, they contribute to the progression of OA by disrupting the metabolic balance in joint tissues by promoting catabolic and anabolic pathways. Their impact on cell joints, as well as the impacts of cell signalling pathways on cytokines and inflammatory substances, determines their function in osteoarthritis development. Apoptosis is evident in osteoarthritic cartilage; however, determining the relative role of chondrocyte apoptosis in the aetiology of OA is difficult, and the rate of apoptotic chondrocytes in osteoarthritic cartilage is inconsistent. The current study summarises the role of apoptosis in the development of osteoarthritis, the mediators, and signalling pathways that trigger the cascade of events, and the other inflammatory features involved.Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.