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Abstract
Ca 2+ 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 Ca 2+ homeostasis is a central cause of contractile dysfunction and arrhythmias in failing myocardium. Defective Ca 2+ homeostasis in heart failure can result from pathological alteration in the expression and activity of an increasingly understood collection of Ca 2+ homeostatic and structural proteins, ion channels, and enzymes. This review focuses on the molecular mechanisms of defective Ca 2+ cycling in heart failure and considers how fundamental understanding of these pathways may translate into novel and innovative therapies.

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