Calmodulin kinase signaling in heart: an intriguing candidate target for therapy of myocardial dysfunction and arrhythmias.
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.
Anderson
Mark E
ME
Vanderbilt University Medical Center, 383 Preston Research Building, Nashville, TN 37232-6300, USA. mark.anderson@vanderbilt.edu
D000818:Animals; D001145:Arrhythmias, Cardiac / Q000188:drug therapy / Q000201:enzymology*; D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2; D017871:Calcium-Calmodulin-Dependent Protein Kinases / Q000037:antagonists & inhibitors* / Q000737:chemistry / Q000502:physiology*; D009202:Cardiomyopathies / Q000188:drug therapy / Q000201:enzymology*; D006801:Humans; D009206:Myocardium / Q000201:enzymology; D015398:Signal Transduction
D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2; D017871:Calcium-Calmodulin-Dependent Protein Kinases