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A growing body of evidence indicates that heart failure progression is tightly associated with dysregulation of phosphorylation of Ca2+ regulators localized in the sub-cellular microdomain of the sarcoplasmic reticulum. Chemical or genetic correction of abnormalities in cardiac phosphorylation cascades is emerging as a potential target in the treatment of heart failure. Here, we review how specific kinases and phosphatases finely tune Ca2+ cycling and regulate excitation-contraction (E-C) coupling in cardiomyocytes.
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