Abstract
The multifunctional Ca(2+)/calmodulin (CaM)-dependent protein kinase II (CaMKII) has emerged as a proarrhythmic and procardiomyopathic signal in a wide range of structural heart diseases. This review discusses CaMKII structure and function and recent evidence implicating CaMKII inhibition as a potential strategy for treating myocardial dysfunction and arrhythmias in the setting of structural heart disease.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, U.S. Gov't, P.H.S.
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Review
MeSH terms
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Animals
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Arrhythmias, Cardiac / drug therapy
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Arrhythmias, Cardiac / enzymology*
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Calcium-Calmodulin-Dependent Protein Kinase Type 2
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Calcium-Calmodulin-Dependent Protein Kinases / antagonists & inhibitors*
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Calcium-Calmodulin-Dependent Protein Kinases / chemistry
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Calcium-Calmodulin-Dependent Protein Kinases / physiology*
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Cardiomyopathies / drug therapy
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Cardiomyopathies / enzymology*
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Humans
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Myocardium / enzymology
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Signal Transduction
Substances
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Calcium-Calmodulin-Dependent Protein Kinase Type 2
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Calcium-Calmodulin-Dependent Protein Kinases