线粒体途径治疗骨关节炎的研究进展

Research progress on mitochondria as targets for osteoarthritis treatment

骨关节炎是以软骨退变及关节间隙变窄为主要特征,普遍存在且具有致残性的关节紊乱。骨关节炎软骨细胞中线粒体功能障碍主要表现为氧化应激反应的增加,线粒体途径细胞凋亡的增加和线粒体自噬的失衡等。本文从以上几方面综述了线粒体功能障碍与骨关节炎的关系以及相应线粒体途径治疗骨关节炎的研究进展,并提出烟酰胺腺嘌呤二核苷酸(NAD+)依赖性蛋白质脱乙酰酶SIRT-3是线粒体途径改善线粒体功能重要的内源性靶分子。此外,我们将近二十年有关线粒体与骨关节炎的研究做了基于共同出现的主题的相关性分析,这将对进一步研究线粒体功能障碍与骨关节炎的关系和线粒体途径治疗骨关节炎的机制研究具有指导意义。

Osteoarthritis(OA)is a common and disabling joint disorder,which is mainly characterized by cartilage degeneration and narrow joint space.Mitochondrial dysfunction in OA chondrocytes is mainly manifested as an increase in oxidative stress,an increase in mitochondrial pathway apoptosis and an imbalance in mitophagy.This article reviews the relationship between mitochondrial dysfunction and OA from the above aspects and the corresponding research progress on mitochondria as targets for OA treatment and proposes that nicotinamide adenine dinucleotide(NAD+)-dependent deacetylases SIRT-3 is a key endogenous target molecular to optimize mitochondrial function.In addition,we made a co-occurrence analysis of mitochondria and OA in the past two decades,which will be of guiding significance for further research on the relationship between mitochondrial dysfunction and OA and the mechanism of mitochondria as targets for OA treatment.