Oxidative stress and diabetic cardiomyopathy: a brief review.
Oxidative stress and diabetic cardiomyopathy: a brief review.
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DOI：
10.1385/ct:1:3:181
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发表时间：
2001-01-01
影响因子：
3.2
通讯作者：
Kang, Y J
中科院分区：
文献类型：
--
作者：
Cai, L;Kang, Y J
糖尿病是一个严重的公共卫生问题。糖尿病非心脏并发症治疗的进步已导致心脏病成为糖尿病患者的主要死亡原因。糖尿病的几种心血管病理后果，如高血压，对心脏有不同程度的影响。然而，高血糖作为一个独立的危险因素，直接导致心脏损害，导致糖尿病心肌病。糖尿病心肌病可以独立于血管疾病发生，尽管其机制在很大程度上尚不清楚。以往的研究很少关注高血糖对心肌细胞的直接影响，大多数研究，特别是体外研究，主要集中在血管平滑肌细胞和内皮细胞致病的分子机制上。因此，迫切需要全面了解糖尿病心肌病的发病机制，以开发预防和治疗糖尿病心脏并发症的方法。本文就糖尿病心肌病的研究现状作一综述。目前的共识是，高血糖导致活性氧和氮的产生，从而导致氧化性心肌损伤。糖尿病晚期会出现心肌结构和功能的改变。这些慢性改变被认为是由于糖尿病早期对突然升高的血糖水平的急性心脏反应造成的。氧化应激是由高血糖产生的活性氧和氮物种引起的，导致基因表达异常，信号转导改变，激活导致心肌细胞程序性死亡的通路。因此，由此导致的心肌细胞丢失在糖尿病心肌病的发展中起着关键作用。靶向预防高血糖引起的氧化性心肌损伤的各种策略的应用进展可能是卓有成效的。
Diabetes is a serious public health problem. Improvements in the treatment of noncardiac complications from diabetes have resulted in heart disease becoming a leading cause of death in diabetic patients. Several cardiovascular pathological consequences of diabetes such as hypertension affect the heart to varying degrees. However, hyperglycemia, as an independent risk factor, directly causes cardiac damage and leads to diabetic cardiomyopathy. Diabetic cardiomyopathy can occur independent of vascular disease, although the mechanisms are largely unknown. Previous studies have paid little attention to the direct effects of hyperglycemia on cardiac myocytes, and most studies, especially in vitro, have mainly focused on the molecular mechanisms underlying pathogenic alterations in vascular smooth-muscle cells and endothelial cells. Thus, a comprehensive understanding of the mechanisms of diabetic cardiomyopathy is urgently needed to develop approaches for the prevention and treatment of diabetic cardiac complications. This review provides a survey of current understanding of diabetic cardiomyopathy. Current consensus is that hyperglycemia results in the production of reactive oxygen and nitrogen species, which leads to oxidative myocardial injury. Alterations in myocardial structure and function occur in the late stage of diabetes. These chronic alterations are believed to result from acute cardiac responses to suddenly increased glucose levels at the early stage of diabetes. Oxidative stress, induced by reactive oxygen and nitrogen species derived from hyperglycemia, causes abnormal gene expression, altered signal transduction, and the activation of pathways leading to programmed myocardial cell deaths. The resulting myocardial cell loss thus plays a critical role in the development of diabetic cardiomyopathy. Advances in the application of various strategies for targeting the prevention of hyperglycemia-induced oxidative myocardial injury may be fruitful.