Key result
Overexpression of PKC beta 2 in transgenic mice markedly reduced cardiomyocyte percentage of shortening compared to wild-type controls (5.2% vs 11.8%) and increased troponin I phosphorylation.
Why the study?
Does PKCbeta2-mediated phosphorylation of troponin I decrease cardiomyocyte calcium responsiveness and contractility in a transgenic mouse model of heart failure?
Population
PKCbeta2 overexpressing transgenic mice (an animal model of heart failure) and wild-type control mice
Comparison
PKCbeta2 overexpression and superfusion of a… vs Wild-type control mice
Design
Preclinical
Authors
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Highlights PKCβ2 as potential target in mouse HF model; leaves open whether inhibition benefits patients.
Does PKCbeta2-mediated phosphorylation of troponin I decrease cardiomyocyte calcium responsiveness and contractility in a transgenic mouse model of heart failure?
Absolute Event Rate: 5.2% vs 11.8%
p-value: p=<0.001
In vivo PKCbeta2-mediated phosphorylation of troponin I decreases myofilament Ca2+ responsiveness and causes cardiomyocyte dysfunction, suggesting PKCbeta inhibition as a potential therapeutic target for heart failure.
Takeishi et al. (1998) studied Heart failure (animal model) (n=11). PKC beta 2 overexpression vs. Wild-type littermates was evaluated on Percentage of cardiomyocyte shortening (p=<0.001). Overexpression of PKC beta 2 in transgenic mice markedly reduced cardiomyocyte percentage of shortening compared to wild-type controls (5.2% vs 11.8%) and increased troponin I phosphorylation.
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