线粒体质量控制在骨性关节炎软骨细胞的调控作用

Regulatory role of mitochondrial quality control in osteoarthritic chondrocytes

软骨退变是骨性关节炎(osteoarthritis, OA)的核心特征,软骨细胞衰老及其介导的代谢失衡是软骨退变持续进展的重要原因。乙酰化/去乙酰化是线粒体质量控制(mitochondrial quality control, MQC)的关键机制之一,主要由去乙酰化酶(sirtuin, SIRT)介导。近年发现MQC失衡与OA软骨细胞衰老及软骨退变密切相关,而SIRT1/3在正常及OA软骨细胞中存在差异表达并参与OA软骨细胞MQC失衡及衰老调控。本文从SIRT1/3及细胞衰老角度对MQC在OA软骨细胞的调控作用做一综述,以期为后续OA发病机制及治疗策略探索整理思路和潜在靶点。

Cartilage degeneration is the core feature of osteoarthritis(OA),while chondrocyte senescence and the related metabolic imbalance are critical reasons for the continuous progression of cartilage degeneration.Acetylation/deacetylation is one of the key mechanisms in mitochondrial quality control(MQC)and is mainly mediated by deacetylase(SIRT).In recent years,it has been found that MQC imbalance is closely related to OA chondrocyte senescence and cartilage degeneration,while SIRT1/3 is differentially expressed in normal and OA chondrocytes,and participates in the regulation of MQC imbalance and senescence of OA chondrocytes.This study reviews the regulatory role of MQC in OA chondrocytes,mainly from the perspective of SIRT1/3 and cellular senescence,to sort out ideas and potential targets for subsequent studies on OA pathogenesis and therapeutics.