Chen Quan, Wu Limin, Dawa Cili, Shen Bin
Department of Orthopedics, Orthopedic Research Institute, West China Hospital, Sichuan University, Chengdu Sichuan, 610041, P. R. China.
Zhongguo Xiu Fu Chong Jian Wai Ke Za Zhi. 2023 Jun 15;37(6):748-757. doi: 10.7507/1002-1892.202303006.
To summarize the role of chondrocyte mitochondrial homeostasis imbalance in the pathogenesis of osteoarthritis (OA) and analyze its application prospects.
The recent literature at home and abroad was reviewed to summarize the mechanism of mitochondrial homeostasis imbalance, the relationship between mitochondrial homeostasis imbalance and the pathogenesis of OA, and the application prospect in the treatment of OA.
Recent studies have shown that mitochondrial homeostasis imbalance, which is caused by abnormal mitochondrial biogenesis, the imbalance of mitochondrial redox, the imbalance of mitochondrial dynamics, and damaged mitochondrial autophagy of chondrocytes, plays an important role in the pathogenesis of OA. Abnormal mitochondrial biogenesis can accelerate the catabolic reaction of OA chondrocytes and aggravate cartilage damage. The imbalance of mitochondrial redox can lead to the accumulation of reactive oxygen species (ROS), inhibit the synthesis of extracellular matrix, induce ferroptosis and eventually leads to cartilage degradation. The imbalance of mitochondrial dynamics can lead to mitochondrial DNA mutation, decreased adenosine triphosphate production, ROS accumulation, and accelerated apoptosis of chondrocytes. When mitochondrial autophagy is damaged, dysfunctional mitochondria cannot be cleared in time, leading to ROS accumulation, which leads to chondrocyte apoptosis. It has been found that substances such as puerarin, safflower yellow, and astaxanthin can inhibit the development of OA by regulating mitochondrial homeostasis, which proves the potential to be used in the treatment of OA.
The mitochondrial homeostasis imbalance in chondrocytes is one of the most important pathogeneses of OA, and further exploration of the mechanisms of mitochondrial homeostasis imbalance is of great significance for the prevention and treatment of OA.
总结软骨细胞线粒体稳态失衡在骨关节炎（OA）发病机制中的作用，并分析其应用前景。
查阅国内外近期文献，总结线粒体稳态失衡的机制、线粒体稳态失衡与OA发病机制的关系以及在OA治疗中的应用前景。
近期研究表明，由软骨细胞线粒体生物发生异常、线粒体氧化还原失衡、线粒体动力学失衡和线粒体自噬受损引起的线粒体稳态失衡在OA发病机制中起重要作用。线粒体生物发生异常可加速OA软骨细胞的分解代谢反应，加重软骨损伤。线粒体氧化还原失衡可导致活性氧（ROS）积累，抑制细胞外基质合成，诱导铁死亡并最终导致软骨降解。线粒体动力学失衡可导致线粒体DNA突变、三磷酸腺苷生成减少、ROS积累以及软骨细胞凋亡加速。当线粒体自噬受损时，功能失调的线粒体无法及时清除，导致ROS积累，进而导致软骨细胞凋亡。已发现葛根素、红花黄色素和虾青素等物质可通过调节线粒体稳态来抑制OA的发展，这证明了其在OA治疗中的应用潜力。
软骨细胞线粒体稳态失衡是OA最重要的发病机制之一，进一步探索线粒体稳态失衡的机制对OA的防治具有重要意义。
