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

摘要:

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 （sir- tuin, 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。

Abstract:

Cartilage degeneration is the core feature of osteoarthritis (OA), while chondrocyte senescence and the related metabolic im- balance 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 imbal- ance 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 regulato- ry 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.