Deletion of the β2-adrenergic receptor prevents the development of cardiomyopathy in mice.

ABSTRACT: Beta adrenergic receptor (β-AR) subtypes act through diverse signaling cascades to modulate cardiac function and remodeling. Previous in vitro studies suggest that β1-AR signaling is cardiotoxic whereas β2-AR signaling is cardioprotective, and may be the case during ischemia/reperfusion in vivo. The objective of this study was to assess whether β2-ARs also play a cardioprotective role in the pathogenesis of non-ischemic forms of cardiomyopathy. To dissect the role of β1 vs β2-ARs in modulating MLP (Muscle LIM Protein) cardiomyopathy, we crossbred MLP-/- with β1-/- or β2-/- mice. Deletion of the β2-AR improved survival, cardiac function, exercise capacity and myocyte shortening; by contrast haploinsufficency of the β1-AR reduced survival. Pathologic changes in Ca(2+) handling were reversed

SUBMITTER: Fajardo G 

PROVIDER: S-EPMC3791213 | biostudies-literature | 2013 Oct

REPOSITORIES: biostudies-literature