Key result
Ruboxistaurin prevented death, reduced ventricular dilation, and enhanced ventricular performance in mice during 10 weeks of pressure-overload stimulation.
Why the study?
Does PKCalpha inhibition with ruboxistaurin improve cardiac contractility and prevent heart failure in mouse models of pressure overload or myocardial infarction?
Population
Wild-type mice and mice lacking PKCalpha, PKCbeta, and PKCgamma subjected to pressure-overload stimulation…
Comparison
Genetic deletion of PKCalpha, PKCbeta, and… vs Wild-type mice; metoprolol treatment
Design
Preclinical
Follow-up
Up to 10 weeks
Authors
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Ruboxistaurin may support PKCα inhibition as a heart failure target; leaves open translation from mouse pressure-overload models to patients.
Does PKCalpha inhibition with ruboxistaurin improve cardiac contractility and prevent heart failure in mouse models of pressure overload or myocardial infarction?
PKCalpha functions distinctly from PKCbeta and PKCgamma in regulating cardiac contractility, and its inhibition with ruboxistaurin represents a potential therapeutic approach for heart failure.
Chen et al. (2009) studied Heart failure. Ruboxistaurin (LY333531) vs. Metoprolol / Control was evaluated on Death and heart failure severity following pressure-overload stimulation. Ruboxistaurin prevented death, reduced ventricular dilation, and enhanced ventricular performance in mice during 10 weeks of pressure-overload stimulation.
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