Population
Cardiomyocytes and mouse models (including Hdac5-null mice)
Comparison
Hypertrophic stresses, histone acetyltransferase… vs Control conditions (untreated or wild-type)
Design
Preclinical
Authors
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Animal data link HDAC2 acetylation to hypertrophy; leaves open human relevance and therapeutic targeting.
This study identifies a novel post-translational mechanism where HDAC2 acetylation, balanced by p300/CBP-associated factor and HDAC5, drives cardiac hypertrophy.
Eom et al. (2014) studied this question.
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