Abstract
Background: Protein phosphatase 1 (PP1) is the negative regulator of cardiac contractility and its activity was shown to be aberrantly upregulated in failing hearts. PP1 catalytic subunits consist of three different genes, PP1α, PP1β, and PP1γ. We previously reported that in vivo knockdown of PP1β was sufficient to augment left ventricular systolic function in normal mice. We herein investigated whether PP1β knockdown halts progression of heart failure in muscle LIM protein deficient cardiomyopathic mice (MLPKO).
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