Osteoarthritis (OA) is a multifactorial arthritic disease of weight-bearing joints concomitant with chronic and intolerable pain, loss of locomotion and impaired quality of life in the elderly population. Although the prevalence of OA increases with age, its specific mechanisms have not been elucidated and effective therapeutic disease-modifying drugs have not been developed. As essential organelles in chondrocytes, mitochondria supply energy and play vital roles in cellular metabolism, proliferation and apoptosis. Mitochondrial quality control (MQC) is the key mechanism to coordinate various mitochondrial biofunctions, primarily through mitochondrial biogenesis, dynamics, autophagy and the newly discovered mitocytosis. An increasing number of studies have revealed that a loss of MQC homeostasis contributes to the cartilage damage during the occurrence and development of OA. Several master MQC-associated signaling pathways and regulators exert chondroprotective roles in OA, while cartilage damage-related molecular mechanisms have been partially identified. In this review, we summarized known mechanisms mediated by dysregulated MQC in the pathogenesis of OA and latent bioactive ingredients and drugs for the prevention and treatment of OA through the maintenance of MQC.

骨关节炎（OA）是一种多因素的负重关节关节炎疾病，伴有慢性和无法忍受的疼痛、运动丧失和老年人群生活质量受损。尽管 OA 的患病率随着年龄的增长而增加，但其具体机​​制尚未阐明，并且尚未开发出有效的治疗疾病改善药物。作为软骨细胞中必不可少的细胞器，线粒体提供能量并在细胞代谢、增殖和凋亡中发挥重要作用。线粒体质量控制 (MQC) 是协调各种线粒体生物功能的关键机制，主要通过线粒体生物发生、动力学、自噬和新发现的有丝分裂。越来越多的研究表明，MQC 稳态的丧失会导致 OA 发生和发展过程中的软骨损伤。几种主要的 MQC 相关信号通路和调节剂在 OA 中发挥软骨保护作用，而软骨损伤相关的分子机制已部分确定。在这篇综述中，我们总结了 MQC 在 OA 发病机制中介导的已知机制以及通过维持 MQC 来预防和治疗 OA 的潜在生物活性成分和药物。