AMPK deficiency in cardiac muscle results in dilated cardiomyopathy in the absence of changes in energy metabolism

Abstract

β1β2M-KO mice display evidence of dilated cardiomyopathy. This is the first mouse model of AMPK deficiency that demonstrates cardiac dysfunction in the absence of pathological stress and provides insights into the role of AMPK in regulating myocardial function, metabolism, hypertrophy, and the progression to heart failure.