线粒体质量控制调控骨质疏松的研究机制进展

摘 要 线粒体是细胞内的信号中枢，在细胞生存、代谢和死亡过程中发挥关键作用。细胞需要维持线粒体的健康状态，并快速修复或清除受损的线粒体，以避免细胞死亡和组织损伤。线粒体质量控制（MQC）机制用于监测和维持线粒体的数量和质量，其中包括线粒体融合和裂变、线粒体生物发生和自噬等过程。骨质疏松症（OP）是一种常见的与衰老相关的疾病，其特征是骨量减少和易碎性骨折。研究发现，线粒体功能障碍在骨质疏松的发展中起着重要作用，线粒体异常功能和数量减少会导致骨细胞代谢紊乱，进而影响骨组织的结构和功能。因此，严格控制线粒体的质量和数量对于预防线粒体损伤对骨质疏松的病理影响至关重要。本综述旨在概述MQC所涉及的分子机制，总结目前MQC在骨质疏松进展中的复杂作用及潜在的治疗策略。

Research Advances in Mitochondrial Quality Control to Regulate Osteoporosis

Mitochondria are signalling hubs within the cell and play an important role in cell survival, metabolism and death. Cells need to maintain mitochondria in a healthy state and to rapidly repair or remove damaged mitochondria to avoid cell death and tissue damage. Mitochondrial quality control (MQC) mechanisms including mitochondrial fusion and fission, mitochondrial biogenesis and autophagy are used to monitor and maintain the quality and quantity of mitochondria. Osteoporosis is a common ageing-related disease characterized by reduced bone mass and fragility fractures. Mitochondrial dysfunction has been found to play an important role in the development of osteoporosis. Abnormal mitochondrial function and reduced numbers lead to disruption of bone cell metabolism, which affects the structure and function of bone tissue. Therefore, strict control of mitochondrial quality and quantity to prevent mitochondrial damage is essential to prevent the pathological effects of osteoporosis. This review aims to provide an overview of the molecular mechanisms involved in MQC, to summarize the complex role of MQC in the progression of osteoporosis, and to explore potential therapeutic strategies.