氧化应激与糖尿病心肌细胞凋亡

Oxidative stress and cardiomyocyte apoptosis in diabetes

氧化应激是糖尿病重要的病理生理过程。氧化应激所导致的心肌细胞凋亡是糖尿病患者非缺血性心力衰竭发生的重要原因。线粒体功能障碍、NADH氧化酶异常以及晚期糖基化终末产物增加是心肌细胞活性氧簇的主要来源。产生的活性氧簇通过直接激活线粒体凋亡途径、肿瘤坏死因子（TNF）α激活死亡受体途径、P53凋亡途径以及p38丝裂原活化蛋白激酶（MAPK）途径，促进心肌细胞凋亡。但是目前针对糖尿病心脏病的抗氧化治疗效果并不理想，因此有必要进一步研究氧化应激导致心肌细胞凋亡的机制，以发现治疗糖尿病心脏病的新方法。

Oxidative stress is an important pathophysiologic process of diabetes. Cardiomyocytes ap- optosis induced by oxidative stress is the important cause of non-ischemia heart failure in patients with diabetes. Disfunction of mitochondria, abnormality of NADH oxidase and increasing of glycosylation end products are the main sources of reactive oxygen species （ROS）. ROS can induce cardiomyocytes apoptosis by mitochondrial apoptosis pathway ,P53-apoptosis pathway, TNF-α death receptor pathway and p38MAPK pathway. But antioxidant therapies for diabetic cardiomyopathy are mild effective recently. It is necessary to understand the nleehanisms of cardiomyocyte apoptosis in diabetes in order to find new therapies.