Mechanisms of altered Ca²⁺ handling in heart failure.
Mechanisms of altered Ca²⁺ handling in heart failure.
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DOI：
10.1161/circresaha.113.301651
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发表时间：
2013-08-30
影响因子：
20.1
通讯作者：
Anderson ME
中科院分区：
文献类型：
--
作者：
Luo M;Anderson ME
Ca ~（2+）在连接心肌细胞膜兴奋性和收缩性中起着至关重要的作用。心力衰竭的标志性特征是机械功能障碍和心律失常;细胞内Ca 2+稳态缺陷是衰竭心肌收缩功能障碍和心律失常的主要原因。心力衰竭中的Ca 2+稳态缺陷可能是由于越来越多地理解的Ca 2+稳态结合蛋白、离子通道和酶的表达和活性的病理改变。本文综述了心力衰竭中Ca 2+循环缺陷的分子机制，并考虑如何将对这些途径的基本理解转化为新的和创新的治疗方法。
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 binding proteins, ion channels and enzymes. This review focuses on the molecular mechanisms of defective Ca2+ cycling in heart failure and consider how fundamental understanding of these pathways may translate into novel and innovative therapies.