Key result
Cardiac-specific overexpression of constitutively active PKCepsilon in transgenic mice caused concentric cardiac hypertrophy with a 28% increase in heart weight and normal in vivo cardiac function.
Why the study?
Does transgenic overexpression of constitutively active PKCepsilon cause cardiac hypertrophy without failure in mice?
Does transgenic overexpression of constitutively active PKCepsilon cause cardiac hypertrophy without failure in mice?
Transgenic overexpression of constitutively active PKCepsilon in mice causes concentric cardiac hypertrophy with preserved in vivo cardiac function, highlighting differential roles of PKC isoforms in heart failure.
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PKCepsilon overexpression may drive adaptive hypertrophy in mice; leaves open isoform-specific roles in human heart failure.
Takeishi et al. (2000) studied Cardiac hypertrophy. Cardiac-specific overexpression of constitutively active PKCepsilon vs. Wild-type mice was evaluated on Cardiac hypertrophy and function. Cardiac-specific overexpression of constitutively active PKCepsilon in transgenic mice caused concentric cardiac hypertrophy with a 28% increase in heart weight and normal in vivo cardiac function.
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