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

被引：181

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

来源：

CELL METABOLISM | 2015年 / 21卷 / 02期

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

页码：183 / 194

页数：12

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