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February 14, 2014Circulation Research

Regulation of Acetylation of Histone Deacetylase 2 by p300/CBP-Associated Factor/Histone Deacetylase 5 in the Development of Cardiac Hypertrophy

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Population

Cardiomyocytes and mouse models (including Hdac5-null mice)

Comparison

Hypertrophic stresses, histone acetyltransferase… vs Control conditions (untreated or wild-type)

Design

Preclinical

Authors

GEGwang Hyeon EomYNYoon Seok NamJOJae Gyun Oh

Discussion

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Overview

Animal data link HDAC2 acetylation to hypertrophy; leaves open human relevance and therapeutic targeting.

Structured PICO

P
Population
Cardiomyocytes and mouse models (including Hdac5-null mice)
I
Intervention
Hypertrophic stresses, histone acetyltransferase inhibitors, nonspecific HDAC inhibitors, and genetic manipulation of Hdac2/Hdac5
C
Comparator
Control conditions (untreated or wild-type)
O
Outcome
Acetylation and enzymatic activity of HDAC2 and development of cardiac hypertrophysurrogate

This study identifies a novel post-translational mechanism where HDAC2 acetylation, balanced by p300/CBP-associated factor and HDAC5, drives cardiac hypertrophy.

Cite This Study

Eom et al. (2014) studied this question.

synapsesocial.com/papers/6a7665e4137c7dcc81bd2dfehttps://doi.org/10.1161/circresaha.114.303429
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