Defective intracellular calcium homeostasis is a central mechanism of contractile dysfunction and arrhythmias in heart failure, representing a potential target for novel therapies.
Supports Ca2+ handling as therapeutic focus in HF; leaves open optimal targets for clinical translation.
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.
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Luo et al. (2013) studied this question.
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