Key result
Minimal transgenic overexpression of p300 induced striking cardiac hypertrophy, whereas heterozygous loss of a single p300 allele reduced pressure overload-induced hypertrophy by approximately 50%.
Why the study?
Does modulation of acetyltransferase p300 levels affect adaptive cardiac hypertrophy in response to hemodynamic loading?
Population
Preclinical models and human heart failure samples
Comparison
Transgenic overexpression of p300 or… vs Wild-type or baseline controls
Design
Preclinical
Authors
Loading...
p300 modulation may limit stress-induced hypertrophy in animals; leaves open therapeutic translation to human heart failure.
Does modulation of acetyltransferase p300 levels affect adaptive cardiac hypertrophy in response to hemodynamic loading?
Small increments in p300 are necessary and sufficient to drive myocardial hypertrophy, suggesting that specific reduction of p300 content or activity may diminish stress-induced hypertrophy and forestall heart failure.
Wei et al. (2008) studied Cardiac hypertrophy and heart failure. p300 overexpression or heterozygous loss vs. Wild-type or normal p300 levels was evaluated on Cardiac hypertrophy and mortality. Minimal transgenic overexpression of p300 induced striking cardiac hypertrophy, whereas heterozygous loss of a single p300 allele reduced pressure overload-induced hypertrophy by approximately 50%.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: