Interplay of Defective Excitation-Contraction Coupling, Energy Starvation, and Oxidative Stress in Heart Failure

被引:18
|
作者
Kohlhaas, Michael [1 ]
Maack, Christoph [1 ]
机构
[1] Univ Klinikum Saarlandes, Med Klin & Poliklin, D-66421 Homburg, Germany
关键词
MITOCHONDRIAL CA2+ UPTAKE; FAILING HUMAN; SARCOPLASMIC-RETICULUM; VENTRICULAR MYOCYTES; INTRACELLULAR CA2+; NA+-CA2+ EXCHANGER; CHANNELS; PROTEIN; MICRODOMAINS; INCREASES;
D O I
10.1016/j.tcm.2012.03.002
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
In chronic heart failure, maladaptive remodeling of the left ventricle (LV) with systolic and diastolic dysfunction underlies the inability of the heart to pump sufficient blood to supply the body with blood and oxygen. Three integral aspects of this maladaptive LV remodeling are (1) defects in excitation-contraction (EC) coupling, particularly of cellular Ca2+ and Na+ homeostasis; (2) an energetic deficit; and (3) oxidative stress. Although these three aspects are often investigated separately from each other, their close and dynamic interplay are increasingly recognized. Central to this novel approach are mitochondria, which are the main source for cellular ATP, but also for reactive oxygen species, and their function is critically regulated by Ca2+ and Na+ Here, we review recent advances in our understanding of how maladaptive changes of EC coupling can contribute to the energetic deficit and oxidative stress, which may initiate a vicious cycle leading to progressive cardiac dysfunction. (Trends Cardiovasc Med 2011;21: 69-73) (C) 2011 Elsevier Inc. All rights reserved.
引用
收藏
页码:69 / 73
页数:5
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