【摘要】 内质网应激（ERS）是细胞对过度的错误折叠或非正确性折叠的蛋白质应激反应，其在骨关节炎（OA）发生发展中的作用机制是近年来研究的热点。ERS可通过促进软骨细胞凋亡、软骨细胞自噬、软骨细胞外基质降解及软骨细胞炎症反应等，促进OA的发生发展。临床可通过药物调节ERS相关信号通路，发挥OA治疗作用。深入研究ERS在OA发生发展中的具体作用机制，可为OA的防治提供新思路。更多还原

【Abstract】 Endoplasmic reticulum stress(ERS) is a cellular response to the accumulation of misfolded or improperly folded proteins. In recent years, the role and mechanisms of ERS in the pathogenesis and progression of osteoarthritis(OA) have garnered significant research attention. ERS can promote the development and progression of OA by inducing chondrocyte apoptosis, chondrocyte autophagy, extracellular matrix degradation, and chondrocyte-mediated inflammatory responses. Clinically, pharmacological modulation of ERS-related signaling pathways has been explored as a therapeutic strategy for OA. In-depth research on the specific mechanism of ERS in the development and progression of OA may provide new ideas for the prevention and treatment of OA.更多还原