中药靶向线粒体质量控制防治骨质疏松症的研究进展

Research progress of mitochondrial quality control against osteoporosis and herbal medicine treatment

关键词:  骨质疏松症  线粒体质量控制  中药  综述

Key words:  osteoporosis  mitochondrial quality control  traditional Chinese medicine  review

摘要:

骨质疏松症（OP）以骨量减少和骨微结构破坏为特征，导致骨折风险增加。传统西医治疗存在长期使用出现不良反应及难以维持骨代谢动态平衡的局限。中药凭借“多靶点、整体调节”的优势，逐渐成为OP防治的新方向。近年研究发现，线粒体质量控制（MQC）机制（包括线粒体生物发生、动力学平衡、氧化应激调控及自噬）在骨代谢稳态中发挥核心作用，其功能紊乱与OP发生密切相关。然而，现有研究多聚焦单一通路或靶点的验证，对MQC系统性调控网络的整体认知仍显不足。因此，文章系统综述中药通过调控MQC防治OP的研究进展，深度解析中药单体及复方在干预线粒体动力学、自噬激活及抗氧化防御中的作用机制，以期为构建“中药-MQC-骨代谢”研究范式提供理论参考，并为开发基于线粒体稳态重塑的精准治疗策略提供理论依据。

Abstract:

Osteoporosis（OP） is characterized by decreased bone mass and destruction of bone microarchitecture，leading to an increased risk of fracture. Traditional Western medical treatments has limitations in terms of long-term use of side effects and maintenance of dynamic balance of bone metabolism. With the advantage of “multi-targeting and overall regulation”，Chinese medicine has gradually become a new direction for OP prevention and treatment. Recent studies have found that the mitochondrial quality control（MQC） mechanism（including mitochondrial biogenesis，kinetic homeostasis，oxidative stress regulation and autophagy） plays a central role in bone metabolism homeostasis，and its dysfunction is closely related to the occurrence of OP. However，existing studies have mostly focused on the validation of single pathways or targets，and the overall knowledge of the systemic regulatory network of MQC is still insufficient. This review systematically synthesizes research progress on Chinese medicine in preventing and treating OP through the regulation of MQC. It delves into the mechanisms by which Chinese medicine monomers and compounds intervene in mitochondrial dynamics，mitophagy activation，and antioxidant defense. The aim is to provide a theoretical reference for establishing the “TCM-MQC-Bone metabolism” research paradigm and to offer a theoretical basis for developing targeted therapeutic strategies based on the remodeling of mitochondrial homeostasis.