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心力衰竭中心脏钙离子处理改变的机制。

Mechanisms of altered Ca²⁺ handling in heart failure.

机构信息

Division of Cardiovascular Medicine, Department of Internal Medicine, Cardiovascular Research Center, Carver College of Medicine, University of Iowa, Iowa City, IA, USA.

出版信息

Circ Res. 2013 Aug 30;113(6):690-708. doi: 10.1161/CIRCRESAHA.113.301651.

Abstract

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.

摘要

钙离子在心肌兴奋-收缩耦联中起着至关重要的作用。心力衰竭的主要特征是机械功能障碍和心律失常;细胞内钙离子稳态失调是心力衰竭心肌收缩功能障碍和心律失常的核心原因。心力衰竭时钙离子稳态失调可导致越来越多的钙离子稳态和结构蛋白、离子通道和酶的表达和活性发生病理性改变。本综述重点讨论心力衰竭时钙离子循环异常的分子机制,并探讨对这些途径的深入了解如何转化为新的创新性治疗方法。

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