Abstract
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.
MeSH terms
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Animals
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Calcium Signaling* / drug effects
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Calcium Signaling* / genetics
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Calcium-Calmodulin-Dependent Protein Kinase Type 2 / metabolism
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Cardiotonic Agents / pharmacology
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Cardiotonic Agents / therapeutic use*
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Cyclic AMP-Dependent Protein Kinases / metabolism
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Disease Progression
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Genetic Therapy / methods*
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Heart Failure / drug therapy
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Heart Failure / genetics
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Heart Failure / metabolism
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Heart Failure / physiopathology
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Heart Failure / therapy*
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Humans
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Myocardial Contraction / drug effects
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Myocardial Contraction / genetics
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Myocytes, Cardiac / drug effects*
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Myocytes, Cardiac / enzymology
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Myocytes, Cardiac / metabolism
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Phosphoric Monoester Hydrolases / genetics
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Phosphoric Monoester Hydrolases / metabolism*
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Phosphorylation
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Protein Kinases / genetics
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Protein Kinases / metabolism*
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Protein Phosphatase 1 / metabolism
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Ryanodine Receptor Calcium Release Channel / metabolism
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Sarcoplasmic Reticulum / drug effects
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Sarcoplasmic Reticulum / metabolism
Substances
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Cardiotonic Agents
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Ryanodine Receptor Calcium Release Channel
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Protein Kinases
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Cyclic AMP-Dependent Protein Kinases
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Calcium-Calmodulin-Dependent Protein Kinase Type 2
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Protein Phosphatase 1
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Phosphoric Monoester Hydrolases