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.
骨关节炎是一种以关节内软骨损伤退变、软骨下骨异常重塑、骨赘生成、滑膜炎症反应和广泛血管生成为特征的慢性退行性关节疾病，是全球60岁以上人群最常见的肌肉骨骼疾病。在骨关节炎的发生发展过程中，软骨细胞的异常代谢发挥了重要致病作用。线粒体功能障碍作为软骨细胞代谢异常的重要诱因，参与了骨关节炎的发生和发展。因此，维持线粒体稳态是一种避免骨关节炎发生的重要方式。线粒体自噬是自噬体靶向吞噬损伤线粒体，以清除受损或功能失调的线粒体，维持线粒体稳态的一种方式。越来越多的研究发现线粒体自噬与骨关节炎密切相关，这提示线粒体自噬功能的调节可以作为一种治疗骨关节炎的新方法。本文通过对近年来线粒体自噬在骨关节炎中的研究进行综述，进一步阐述了线粒体自噬调控骨关节炎的潜在机制，为线粒体自噬治疗骨关节炎的相关研究提供理论依据。.
骨关节炎是一种以关节内软骨损伤退变、软骨下骨异常重塑、骨赘生成、滑膜炎症反应和广泛血管生成为特征的慢性退行性关节疾病，是全球60岁以上人群最常见的肌肉骨骼疾病。在骨关节炎的发生发展过程中，软骨细胞的异常代谢发挥了重要致病作用。线粒体功能障碍作为软骨细胞代谢异常的重要诱因，参与了骨关节炎的发生和发展。因此，维持线粒体稳态是一种避免骨关节炎发生的重要方式。线粒体自噬是自噬体靶向吞噬损伤线粒体，以清除受损或功能失调的线粒体，维持线粒体稳态的一种方式。越来越多的研究发现线粒体自噬与骨关节炎密切相关，这提示线粒体自噬功能的调节可以作为一种治疗骨关节炎的新方法。本文通过对近年来线粒体自噬在骨关节炎中的研究进行综述，进一步阐述了线粒体自噬调控骨关节炎的潜在机制，为线粒体自噬治疗骨关节炎的相关研究提供理论依据。
Keywords: Apoptosis; Chondrocyte; Mitochondria; Mitophagy; Osteoarthritis.