Cell Death and Diabetic Cardiomyopathy

被引:208
作者
Lu Cai
Y. James Kang
机构
[1] Department of Medicine, University of Louisville, Louisville
[2] Dept. of Pharmacology and Toxicology, University of Louisville, Louisville
[3] Jewish Hosp. Heart and Lung Inst., Louisville
[4] Department of Medicine, Univ. of Louisville Sch. of Medicine, Louisville
基金
美国国家卫生研究院;
关键词
Antioxidants; Apoptosis; Cytokines; Hyperglycemia; Hyperlipidemia; Inflammation; Oxidative stress;
D O I
10.1385/CT:3:3:219
中图分类号
学科分类号
摘要
Myocardial cell death is a key element in the pathogenesis and progression of various etiological cardiomyopathies such as ischemia-reperfusion, toxic exposure, and various chronic diseases including myocardial infarction, atherosclerosis, and endothelial dysfunction. Myocardial cell death is also observed in the hearts of diabetic patients and animal models; however, its importance in the development of diabetic cardiomyopathy is not completely understood. The goal of this review is to summarize our current understanding of the characteristics of diabetes-induced myocardial cell death. In the search of the mechanisms by which diabetes induces myocardial cell death, multiple cell death pathways have been proposed. Reactive oxygen and nitrogen species accumulation plays a critical role in the cell death process. Several studies have shown that suppression of myocardial cell death by antioxidants or inhibitors for apoptosis-specific signaling pathways results in a significant prevention of diabetic cardiotoxicity, suggesting that cell death in diabetic subjects plays an important role in the development of diabetic cardiomyopathy.
引用
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页码:219 / 228
页数:9
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