Mechanisms of Altered Ca2+ Handling in Heart Failure

被引：336

作者：

Luo, Min ^{[1
]}

Anderson, Mark E. ^{[1
,2
]}

机构：

[1] Univ Iowa, Dept Internal Med, Cardiovasc Res Ctr, Div Cardiovasc Med, Iowa City, IA 52242 USA

[2] Univ Iowa, Carver Coll Med, Dept Mol Physiol & Biophys, Iowa City, IA USA

来源：

CIRCULATION RESEARCH | 2013年 / 113卷 / 06期

基金：

美国国家卫生研究院;

关键词：

calcium; CaMKII; excitation-contraction coupling; heart failure; mitochondria; CA2+/CALMODULIN-DEPENDENT PROTEIN-KINASE; CARDIAC RYANODINE RECEPTOR; BETA-ADRENERGIC-RECEPTOR; LEFT-VENTRICULAR DYSFUNCTION; TRIGGERED PROPAGATED CONTRACTIONS; FORCE-FREQUENCY-RELATIONSHIP; II INHIBITION PROTECTS; K-ATP CHANNELS; SARCOPLASMIC-RETICULUM; MITOCHONDRIAL CA2+;

D O I：

10.1161/CIRCRESAHA.113.301651

中图分类号：

R5 [内科学];

学科分类号：

100201 [内科学];

摘要：

Ca2+ plays a crucial role in connecting membrane excitability with contraction in myocardium. The hallmark features of heart failure are mechanical dysfunction and arrhythmias; defective intracellular Ca2+ homeostasis is a central cause of contractile dysfunction and arrhythmias in failing myocardium. Defective Ca2+ homeostasis in heart failure can result from pathological alteration in the expression and activity of an increasingly understood collection of Ca2+ homeostatic and structural proteins, ion channels, and enzymes. This review focuses on the molecular mechanisms of defective Ca2+ cycling in heart failure and considers how fundamental understanding of these pathways may translate into novel and innovative therapies.

引用

页码：690 / 708

页数：19

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