软骨细胞线粒体功能异常对骨关节炎发病机制的研究

Research progress of cartilage mitochondrial dysfunction in osteoarthritis

骨关节炎(osteoarthritis, OA)主要是关节软骨退变导致的慢性炎症性关节疾病,病因及发病机制复杂,最新研究发现,软骨细胞中的线粒体功能异常与OA发病机制密切相关。线粒体通过调控软骨细胞衰老、凋亡、氧化应激、炎症抑制,参与OA发病进程。此外,线粒体相关信号通路AMPK/SIRT3对于调节软骨细胞的代谢过程很重要,表明这些可能是OA治疗的目标。因此,该文论述软骨细胞线粒体功能异常与OA的发病机制的相关性。

Osteoarthritis(OA)is a chronic inflammatory joint disease caused by the degeneration of articular cartilage.Its etiology and pathogenesis are complex.The latest research shows that the mitochondrial dysfunction in chondrocytes is closely related to the pathogenesis of OA.Mitochondria participate in the pathogenesis of OA by regulating the aging,apoptosis,oxidative stress and inflammation inhibition of chondrocytes.In addition,the mitochondrial signal pathway AMPK/SIRT3 is important for regulating the metabolic process of chondrocytes,which indicates that these may be the targets of OA treatment.Therefore,this paper discusses the correlation between abnormal mitochondrial function of chondrocytes and the pathogenesis of OA.