【摘要】 线粒体是人体中不可或缺的细胞器，在能量代谢和信号传导中发挥着重要作用。遗传突变、环境毒素作用、氧化应激和细胞衰老等因素可能导致线粒体损伤，继而引起细胞能量供应不足、增殖能力受损等。线粒体损伤具有双重作用：轻度损伤时，线粒体在代谢应激下通过AMP活化蛋白激酶等信号通路激活生物发生与自噬，促进修复；重度损伤时，则通过多种机制引起细胞损伤甚至死亡。诸多研究已证实，线粒体损伤影响着诸多器官如肝脏、心脏、神经等的组织修复进程，为此研究者开发了多种线粒体保护策略。本文综述线粒体损伤在组织修复中的双重作用及其分子机制，以及靶向线粒体损伤的治疗策略的研究进展。更多还原

【Abstract】 Mitochondria are indispensable organelles in the human body, playing crucial roles in energy metabolism and signal transduction. Genetic mutations, environmental toxin exposure, oxidative stress, and cellular senescence can induce mitochondrial dysfunction, which in turn leads to insufficient cellular energy supply and impaired proliferative capacity. Mitochondrial damage exerts a dual effect: under mild damage conditions, mitochondria can sense metabolic stress through signaling pathways such as AMP-activated protein kinase, activating biogenesis and autophagic mechanisms to achieve self-repair; in cases of severe damage, however, it triggers cellular dysfunction and even programmed cell death through multiple pathways. Numerous studies have demonstrated that mitochondrial damage significantly affects the tissue repair processes of multiple organs including the liver, heart, and nervous system. Therefore, intervention strategies targeting mitochondrial protection have become a research focus. This review summarizes the dual roles of mitochondrial damage in tissue repair and their underlying molecular mechanisms, as well as the research progress of therapeutic strategies targeting mitochondrial damage.更多还原