Abstract
Calcium (Ca2+) is a key player in cardiomyocyte homeostasis, and its roles span from excitation-contraction coupling to metabolic and structural signaling. Alterations in the function or expression of Ca2+-handling proteins are common findings in failing cardiomyocytes, which have been linked to impaired contractility and detrimental remodeling of the cellular structure. For these reasons, the study of intracellular Ca2+ handling in cardiomyocytes represents a central method in experimental molecular cardiology.
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