Altered Myocardial Calcium Cycling and Energetics in Heart Failure-A Rational Approach for Disease Treatment

被引:173
|
作者
Gorski, Przemek A. [1 ]
Ceholski, Delaine K. [1 ]
Hajjar, Roger J. [1 ]
机构
[1] Mt Sinai Hosp, Icahn Sch Med, Cardiovasc Res Ctr, New York, NY 10029 USA
基金
美国国家卫生研究院;
关键词
SARCOPLASMIC-RETICULUM CA2+-ATPASE; MITOCHONDRIAL PERMEABILITY TRANSITION; POLYMORPHIC VENTRICULAR-TACHYCARDIA; CARDIAC RYANODINE RECEPTORS; HUMAN PHOSPHOLAMBAN GENE; CA-BINDING-PROTEIN; RELEASE CHANNEL; HISTIDINE-RICH; DILATED CARDIOMYOPATHY; PKA PHOSPHORYLATION;
D O I
10.1016/j.cmet.2015.01.005
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Cardiomyocyte function depends on coordinated movements of calcium into and out of the cell and the proper delivery of ATP to energy-utilizing enzymes. Defects in calcium-handling proteins and abnormal energy metabolism are features of heart failure. Recent discoveries have led to gene-based therapies targeting calcium-transporting or -binding proteins, such as the cardiac sarco(endo) plasmic reticulum calcium ATPase (SERCA2a), leading to improvements in calcium homeostasis and excitation-contraction coupling. Here we review impaired calcium cycling and energetics in heart failure, assessing their roles from both a mutually exclusive and interdependent viewpoint, and discuss therapies that may improve the failing myocardium.
引用
收藏
页码:183 / 194
页数:12
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