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

作　　者：陈欣[1,2] 刘建军 谢兴文 王多贤[2] 安文博 罗鹏飞 CHEN Xin;LIU Jianjun;XIE Xingwen;WANG Duoxian;AN Wenbo;LUO Pengfei(Gansu University of Traditional Chinese Medicine,Lanzhou 730000,China;Affiliated Hospital of Gansu University of Traditional Chinese Medicine,Lanzhou 730000,China)

机构地区：[1]甘肃中医药大学,甘肃兰州730000 [2]甘肃中医药大学附属医院,甘肃兰州730000

出　　处：《中国骨质疏松杂志》2023年第6期875-880,共6页Chinese Journal of Osteoporosis

基　　金：2020年兰州市人才创新创业项目(2020-RC-64);2020年甘肃省青年科技基金(20JRTORA345);兰州市城关区科技计划项目(2020-2-2-7);2021年卫生健康行业科研项目(GSWSKJ-2021-009);兰州市科技发展指导性计划项目(2020-ZD-65)。

摘　　要：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.

关 键 词：骨关节炎 线粒体 炎症小体 软骨细胞 

分 类 号：R589.5[医药卫生—内分泌]