Abstract
Calcium (Ca2+) plays a critical role in cardiac function. Abnormalities in cardiomyocyte intracellular Ca2+ dynamics contribute to the pathophysiological changes observed in several cardiac diseases including cardiac hypertrophy, chronic heart failure, ventricular arrhythmias, and vascular remodeling. In addition to its key role in maintaining cardiac excitation–contraction coupling, it is increasingly apparent that changes in myocardial Ca2+ also contribute to the regulation of normal and pathological signal transduction that controls myocyte growth, hypertrophic signaling, and transcriptional gene expression. Interestingly, experimental evidence suggests that these multifarious Ca2+-dependent responses are spatially and temporally mediated by distinct cellular Ca2+ pools (i.e., microdomains) which are generated by diverse channels, calcium-binding proteins, and molecular signals with widely differing timescales of activation and localization. These concepts will be discussed in this chapter alongside the emerging role of endoplasmic reticulum stress in myocardial Ca2+ dynamics and cardiac physiology.
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