Diabetic cardiomyopathy and metabolic remodeling of the heart

被引:74
作者
Battiprolu, Pavan K. [1 ]
Lopez-Crisosto, Camila [3 ,4 ]
Wang, Zhao V. [1 ]
Nemchenko, Andriy [1 ]
Lavandero, Sergio [1 ,3 ,4 ]
Hill, Joseph A. [1 ,2 ]
机构
[1] Univ Texas SW Med Ctr Dallas, Dept Internal Med Cardiol, Dallas, TX 75235 USA
[2] Univ Texas SW Med Ctr Dallas, Dept Mol Biol, Dallas, TX 75235 USA
[3] Univ Chile, Fac Ciencias Quim & Farmaceut, Ctr Estudios Mol Celula, Santiago 8380492, Chile
[4] Univ Chile, Fac Med, Santiago 8380492, Chile
关键词
Diabetic cardiomyopathy; Insulin resistance; Heart; Metabolism; FoxO; mTOR; UNFOLDED PROTEIN RESPONSE; ENDOPLASMIC-RETICULUM STRESS; ADIPOSE-TISSUE; PIM-1; KINASE; CARDIAC-HYPERTROPHY; INSULIN-RESISTANCE; GENE-TRANSFER; IN-VIVO; DYSFUNCTION; GROWTH;
D O I
10.1016/j.lfs.2012.10.011
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
The incidence and prevalence of diabetes mellitus are both increasing rapidly in societies around the globe. The majority of patients with diabetes succumb ultimately to heart disease, much of which stems from atherosclerotic disease and hypertension. However, the diabetic milieu is itself intrinsically noxious to the heart, and cardiomyopathy can develop independent of elevated blood pressure or coronary artery disease. This process, termed diabetic cardiomyopathy, is characterized by significant changes in the physiology, structure, and mechanical function of the heart. Presently, therapy for patients with diabetes focuses largely on glucose control, and attention to the heart commences with the onset of symptoms. When the latter develops, standard therapy for heart failure is applied. However, recent studies highlight that specific elements of the pathogenesis of diabetic heart disease are unique, raising the prospect of diabetes-specific therapeutic intervention. Here, we review recently unveiled insights into the pathogenesis of diabetic cardiomyopathy and associated metabolic remodeling with an eye toward identifying novel targets with therapeutic potential. Published by Elsevier Inc.
引用
收藏
页码:609 / 615
页数:7
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