Molecular mechanisms of diabetic cardiomyopathy

被引:810
作者
Bugger, Heiko [1 ]
Abel, E. Dale [2 ]
机构
[1] Univ Freiburg, Ctr Heart, D-79106 Freiburg, Germany
[2] Univ Iowa, Fraternal Order Eagles Diabet Res Ctr, Div Endocrinol & Metab, Roy J & Lucille A Carver Coll Med, Iowa City, IA 52242 USA
基金
美国国家卫生研究院;
关键词
Animal models; Autophagy; Cardiomyopathy; Diabetes; Fibrosis; Heart failure; Inflammation; Lipotoxicity; Metabolism; Review; ENDOPLASMIC-RETICULUM STRESS; MYOCARDIAL MITOCHONDRIAL DYSFUNCTION; PREVENTS LIPOTOXIC CARDIOMYOPATHY; LEFT-VENTRICULAR DYSFUNCTION; IMPAIRS GLUCOSE-METABOLISM; ACTIVATED PROTEIN-KINASE; SYNTHASE TRANSGENIC MICE; NADPH OXIDASE ACTIVATION; GLYCATION END-PRODUCTS; FATTY-ACID OXIDATION;
D O I
10.1007/s00125-014-3171-6
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
In recent years, diabetes mellitus has become an epidemic and now represents one of the most prevalent disorders. Cardiovascular complications are the major cause of mortality and morbidity in diabetic patients. While ischaemic events dominate the cardiac complications of diabetes, it is widely recognised that the risk for developing heart failure is also increased in the absence of overt myocardial ischaemia and hypertension or is accelerated in the presence of these comorbidities. These diabetes-associated changes in myocardial structure and function have been called diabetic cardiomyopathy. Numerous molecular mechanisms have been proposed to contribute to the development of diabetic cardiomyopathy following analysis of various animal models of type 1 or type 2 diabetes and in genetically modified mouse models. The steady increase in reports presenting novel mechanistic data on this subject expands the list of potential underlying mechanisms. The current review provides an update on molecular alterations that may contribute to the structural and functional alterations in the diabetic heart.
引用
收藏
页码:660 / 671
页数:12
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