Wang Yan, Li Jialin, Zhang Ziyi, Wang Runzi, Bo Hai, Zhang Yong
Tianjin Key Laboratory of Exercise Physiology and Sports Medicine, School of Exercise and Health, Tianjin University of Sport, Tianjin 301617, China.
School of Physical Education, Guangdong Institute of Petrochemical Technology, Maoming 525000, China.
Life (Basel). 2023 Apr 13;13(4):1006. doi: 10.3390/life13041006.
The mitochondrial unfolded protein response (UPRmt) and mitophagy are two mitochondrial quality control (MQC) systems that work at the molecular and organelle levels, respectively, to maintain mitochondrial homeostasis. Under stress conditions, these two processes are simultaneously activated and compensate for each other when one process is insufficient, indicating mechanistic coordination between the UPRmt and mitophagy that is likely controlled by common upstream signals. This review focuses on the molecular signals regulating this coordination and presents evidence showing that this coordination mechanism is impaired during aging and promoted by exercise. Furthermore, the bidirectional regulation of reactive oxygen species (ROS) and AMPK in modulating this mechanism is discussed. The hierarchical surveillance network of MQC can be targeted by exercise-derived ROS to attenuate aging, which offers a molecular basis for potential therapeutic interventions for sarcopenia.
线粒体未折叠蛋白反应（UPRmt）和线粒体自噬是两个线粒体质量控制（MQC）系统，分别在分子和细胞器水平发挥作用，以维持线粒体稳态。在应激条件下，这两个过程同时被激活，当一个过程不足时它们会相互补偿，这表明UPRmt和线粒体自噬之间存在机制协调，而这种协调可能由共同的上游信号控制。本综述重点关注调节这种协调的分子信号，并提供证据表明这种协调机制在衰老过程中受损，而运动可促进其恢复。此外，还讨论了活性氧（ROS）和AMPK在调节这一机制中的双向调节作用。运动产生的ROS可以靶向MQC的分级监测网络以减轻衰老，这为少肌症的潜在治疗干预提供了分子基础。
