《生命科学》 2025, 37(2): 130-139
运动调控线粒体功能改善糖尿病心肌病的研究进展
摘 要：
作为糖尿病的并发症，糖尿病心肌病(diabetic cardiomyopathy, DCM) 是一种排除高血压病、冠状动脉疾病和瓣膜病变的心室舒张或收缩功能障碍的疾病。DCM 长期发展可能导致心衰，危害患者的身体健康。线粒体不仅在心肌细胞内提供能量，而且还直接参与DCM 的发生和发展，其功能的正常运作对机体保持正常的心肌功能十分重要。本文主要对DCM 相关的线粒体功能异常的表现和机制，以及运动调控线粒体功能改善DCM 的机制进行综述。结果发现线粒体功能障碍与DCM 的发展存在密切联系，线粒体自噬障碍、线粒体动力学失衡、线粒体生物合成紊乱、线粒体氧化应激、Ca2+ 调节异常以及能量代谢异常等都会导致DCM，而不同的运动方式可以调节线粒体功能，延缓DCM 的发生和发展。本文为DCM 的治疗提供了新的靶点和通路，为科学制定DCM 的运动处方提供了理论依据。
通讯作者：王孝文 , Email:wangxiaowen2003@163.com 孙忠广 , Email:sunzhongguang@outlook.com
Abstract:
As a complication of diabetes, diabetic cardiomyopathy (DCM) is a condition characterized by
ventricular diastolic or systolic dysfunction that occurs independently of hypertension, coronary artery disease, and valvular heart disease. Long-term progression of DCM may lead to heart failure, adversely affecting the health. Mitochondria not only supply energy to myocardial cells but also play a direct role in the onset and progression of DCM. Proper mitochondrial function is crucial for maintaining normal myocardial activity. This review focuses on the manifestation and mechanism of mitochondrial function abnormalities associated with DCM and explores the mechanisms of exercise-regulated mitochondrial function to improve DCM. The findings indicate that mitochondrial dysfunction is closely associated with the development of DCM, and mitochondrial autophagy disorder, imbalance of mitochondrial dynamics, mitochondrial biosynthesis disorder, mitochondrial oxidative stress, abnormal Ca2+regulation and energy metabolism may contribute to its onset. Furthermore, various forms of physical activity can modulate mitochondrial functions, potentially delaying the onset and progression of DCM. This paper may identify new targets and pathways for DCM treatment and provide a theoretical foundation for the scientific formulating exercise prescription on DCM.
Communication Author：WANG Xiao-Wen , Email:wangxiaowen2003@163.com SUN Zhong-Guang , Email:sunzhongguang@outlook.com
