Department of Sport Rehabilitation, Shanghai University of Sport, Shanghai 200438, China.
National Key Laboratory of Immunity and Inflammation, Naval Medical University, Shanghai 200433, China.
J Zhejiang Univ Sci B. 2024 Mar 15;25(3):197-211. doi: 10.1631/jzus.B2300402.
Osteoarthritis (OA), characterized by cartilage degeneration, synovial inflammation, and subchondral bone remodeling, is among the most common musculoskeletal disorders globally in people over 60 years of age. The initiation and progression of OA involves the abnormal metabolism of chondrocytes as an important pathogenic process. Cartilage degeneration features mitochondrial dysfunction as one of the important causative factors of abnormal chondrocyte metabolism. Therefore, maintaining mitochondrial homeostasis is an important strategy to mitigate OA. Mitophagy is a vital process for autophagosomes to target, engulf, and remove damaged and dysfunctional mitochondria, thereby maintaining mitochondrial homeostasis. Cumulative studies have revealed a strong association between mitophagy and OA, suggesting that the regulation of mitophagy may be a novel therapeutic direction for OA. By reviewing the literature on mitophagy and OA published in recent years, this paper elaborates the potential mechanism of mitophagy regulating OA, thus providing a theoretical basis for studies related to mitophagy to develop new treatment options for OA.
骨关节炎(OA)以软骨退变、滑膜炎症和软骨下骨重塑为特征,是全球 60 岁以上人群中最常见的肌肉骨骼疾病之一。OA 的发生和发展涉及软骨细胞的异常代谢,这是一个重要的致病过程。软骨退变的特征是线粒体功能障碍,这是异常软骨细胞代谢的一个重要致病因素。因此,维持线粒体的动态平衡是减轻 OA 的重要策略。自噬体靶向、吞噬和清除受损和功能失调的线粒体的重要过程是线粒体自噬。累积的研究表明,线粒体自噬与 OA 之间存在强烈的关联,这表明调节线粒体自噬可能是 OA 的一种新的治疗方向。通过回顾近年来关于线粒体自噬与 OA 的文献,本文阐述了线粒体自噬调节 OA 的潜在机制,从而为与线粒体自噬相关的研究提供了理论依据,以开发 OA 的新治疗选择。