骨关节炎与衰老相关的发病机制  

Aging-related Pathogenesis of Osteoarthritis

作　　者：文晨曦 李敬扬[1] 文振华[1] WEN Chenxi;LI Jingyang;WEN Zhenhua(Department of Rheumatology and Immunology,Zhuzhou Hospital Affiliated to Xiangya School of Medicine,Central South University,Zhuzhou 412000,China;Central South University,Changsha 410000,China)

机构地区：[1]中南大学湘雅医学院附属株洲医院风湿免疫科,湖南株洲412000 [2]中南大学,长沙410000

出　　处：《医学综述》2022年第10期1911-1916,共6页Medical Recapitulate

摘　　要：骨关节炎(OA)是临床常见的关节疾病之一,其病因及发病机制尚不完全清楚。衰老会导致机体的形态结构和生理功能出现一系列慢性、进行性、退化性的变化,其参与骨关节疾病的发病,目前已知的与衰老相关的OA发病机制包括衰老细胞堆积、表观遗传学修饰、氧化应激和线粒体功能障碍以及细胞死亡等。线粒体自噬在维持软骨细胞稳态中有重要作用,线粒体自噬受损将导致受损线粒体清除受限,进而导致OA发病;细胞坏死和凋亡也促进了OA的发生。深入研究与衰老相关的发病机制可为OA的早期治疗提供新的作用靶点。Osteoarthritis(OA)is one of the common clinical joint diseases,and its etiology and pathogenesis are not fully understood.Aging will lead to a series of chronic,progressive and degenerative changes in the body′s morphological structure and physiological function,which are involved in the pathogenesis of bone and joint diseases.The currently known aging-related mechanisms of osteoarthritis include the accumulation of senescent cells,epigenetic modifications,oxidative stress and mitochondrial dysfunction,and cell death.Mitophagy plays an important role in maintaining chondrocyte homeostasis.Impaired mitophagy will result in restricted clearance of damaged mitochondria,leading to the onset of OA.Cell necrosis and apoptosis also promote the occurrence of OA.In-depth study of the pathogenesis related to aging can provide new targets for the early treatment of OA.

关 键 词：骨关节炎 衰老 发病机制 治疗靶点 

分 类 号：R684.3[医药卫生—骨科学]