氧化应激与自噬相互作用在糖尿病心肌病发病中的研究现状

Roles of Interplay between Oxidative Stress and Autophagy in the Development of Diabetic Cardiomyopathy

糖尿病心肌病是糖尿病引起的一种心血管并发症。越来越多的实验证据表明,氧化应激与自噬的复杂相互关系在糖尿病心血管并发症中起到关键作用。高糖血症及血糖水平波动引起线粒体产生活性氧簇增多,可诱发心肌细胞急性氧化应激,导致心肌病理性变化,最终引起心肌收缩和舒张功能障碍。线粒体氧化应激的增强是糖尿病心血管并发症的始动因素。此外,氧化应激状态会导致线粒体等细胞器损伤和脂质过氧化,促进细胞自噬、线粒体自噬而参与糖尿病心肌病的发生发展。因此,彻底认识及理解氧化应激与自噬相互关系在糖尿病心肌病发病中的作用,在糖尿病心肌病的早期预防及治疗方面有着重大意义。

Diabetic cardiomyopathy is one of the cardiovascular complications of diabetes.There is growing experimental evidence that the complex interplay of oxidative stress and autophagy plays an important role in diabetic cardiovascular complications.Hyperglycemia and fluctuating glucose levels increase production of reactive oxygen species （ ROS ） from the mitochondria, which can induce acute oxidative stress in myocardial cell, and promote cardiac pathological remodeling, and then lead to myocardial systolic and diastolic dysfunction in the end.Elevated oxidative stress in mitochondria is the primary causes of diabetic cardiomyopathy.In addition, the increased activity of damaged organelles such as mitochondria and lipid peroxidation can induces autophagy and mitochondrial autophagy during oxidative stress, which participate in the development of diabetic cardiomyopathy. Therefore, more thorough understanding the complex interplay of oxidative stress with autophagy is critical significantly for the early prevention and treatment of diabetic cardiomyopathy.