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Calmodulin kinase II inhibition protects against structural heart disease
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Journal Article
Calmodulin kinase II inhibition protects against structural heart disease
2005
Overview
β-Adrenergic receptor (βAR) stimulation increases cytosolic Ca
2+
to physiologically augment cardiac contraction, whereas excessive βAR activation causes adverse cardiac remodeling, including myocardial hypertrophy, dilation and dysfunction, in individuals with myocardial infarction. The Ca
2+
-calmodulin–dependent protein kinase II (CaMKII) is a recently identified downstream element of the βAR-initiated signaling cascade that is linked to pathological myocardial remodeling and to regulation of key proteins involved in cardiac excitation-contraction coupling. We developed a genetic mouse model of cardiac CaMKII inhibition to test the role of CaMKII in βAR signaling
in vivo
. Here we show CaMKII inhibition substantially prevented maladaptive remodeling from excessive βAR stimulation and myocardial infarction, and induced balanced changes in excitation-contraction coupling that preserved baseline and βAR-stimulated physiological increases in cardiac function. These findings mark CaMKII as a determinant of clinically important heart disease phenotypes, and suggest CaMKII inhibition can be a highly selective approach for targeting adverse myocardial remodeling linked to βAR signaling.
Publisher
Nature Publishing Group US,Nature Publishing Group
Subject
Adrenergic beta-Antagonists - pharmacology
/ Animals
/ Arrhythmias, Cardiac - metabolism
/ Biomedical and Life Sciences
/ Calcium-Calmodulin-Dependent Protein Kinase Type 2
/ Calcium-Calmodulin-Dependent Protein Kinases - antagonists & inhibitors
/ Calcium-Calmodulin-Dependent Protein Kinases - physiology
/ Kinases
/ Medicine
/ Mice
/ Myocardial Infarction - metabolism
/ Myocardial Infarction - physiopathology
/ Peptides
/ Proteins
