线粒体动力学失衡在糖尿病心肌缺血再灌注损伤中的作用

Role of mitochondrial dynamics imbalance in diabetic myocardial ischemia/reperfusion injury

缺血性心脏病是糖尿病患者死亡的重要原因,恢复缺血心肌组织灌注是其根本治疗措施,但可导致心肌缺血再灌注损伤。线粒体稳态对高能量需求的心肌细胞的正常生理活动有重要意义。线粒体稳态的维持依赖于线粒体融合和分裂即线粒体动力学。糖尿病时,糖脂代谢紊乱可导致线粒体动力学相关蛋白的变化,引起线粒体动力学失衡,从而导致糖尿病心肌细胞线粒体功能障碍,促进糖尿病缺血性心脏病的发生、发展,其机制可能与活性氧爆发、钙超载、线粒体通透性转换孔开放、自噬紊乱、内质网应激、细胞凋亡及焦亡等有关。本文就线粒体动力学在糖尿病心肌缺血再灌注损伤中作用的研究进展作一综述。

Ischemic cardiomyopathy is an important cause of death in diabetic patients. Restoring ischemic myocardial tissue perfusion is the fundamental treatment, but this process will lead to myocardial ischemia/reperfusion injury. Mitochondrial homeostasis is of great importance for normal cell physiology, especially in cardiomyocytes with high energy demands. Mitochondria continue to undergo a process of fusion and fission, that is, mitochondrial dynamics, which is essential for maintaining mitochondrial homeostasis. However, in the state of diabetes, disorders of glucose and lipid metabolism can lead to changes in mitochondrial dynamics-related proteins and cause mitochondrial dynamics imbalance, which leads to mitochondrial dysfunction in diabetic cardiomyocytes, and ultimately promotes the development of diabetic ischemic heart disease. The mechanism may be correlated with oxidative stress, calcium overload, mitochondrial permeability transition pore opening, autophagy disorder, endoplasmic reticulum stress, cell apoptosis and pyrolysis. This paper reviews the research progress of the role of mitochondrial dynamics in diabetic myocardial ischemia/reperfusion injury.