Mitochondrial dysfunction in diabetic cardiomyopathy

被引:164
作者
Duncan, Jennifer G. [1 ]
机构
[1] Washington Univ, Sch Med, Dept Pediat, St Louis, MO 63110 USA
来源
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH | 2011年 / 1813卷 / 07期
关键词
Diabetes; Insulin resistance; Heart failure; Cardiomyopathy; Mitochondria; Oxidative stress; Metabolism; ACTIVATED RECEPTOR-ALPHA; MYOCARDIAL SUBSTRATE METABOLISM; FATTY-ACID OXIDATION; TRANSCRIPTIONAL COACTIVATOR PGC-1-ALPHA; REDUCED CARDIAC EFFICIENCY; GLYCATION END-PRODUCTS; PPAR-ALPHA; INSULIN-RESISTANCE; UNCOUPLING PROTEINS; ENERGY-METABOLISM;
D O I
10.1016/j.bbamcr.2011.01.014
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Cardiovascular disease is common in patients with diabetes and is a significant contributor to the high mortality rates associated with diabetes. Heart failure is common in diabetic patients, even in the absence of coronary artery disease or hypertension, an entity known as diabetic cardiomyopathy. Evidence indicates that myocardial metabolism is altered in diabetes, which likely contributes to contractile dysfunction and ventricular failure. The mitochondria are the center of metabolism, and recent data suggests that mitochondrial dysfunction may play a critical role in the pathogenesis of diabetic cardiomyopathy. This review summarizes many of the potential mechanisms that lead to mitochondrial dysfunction in the diabetic heart. This article is part of a Special Issue entitled: Mitochondria and Cardioprotection. (C) 2011 Elsevier B.V. All rights reserved.
引用
收藏
页码:1351 / 1359
页数:9
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