Suppression of class I and II histone deacetylases blunts pressure-overload cardiac hypertrophy.

ABSTRACT:

Background

Recent work has demonstrated the importance of chromatin remodeling, especially histone acetylation, in the control of gene expression in the heart. In cell culture models of cardiac hypertrophy, pharmacological suppression of histone deacetylases (HDACs) can either blunt or amplify cell growth. Thus, HDAC inhibitors hold promise as potential therapeutic agents in hypertrophic heart disease.

Methods and results

In the present investigation, we studied 2 broad-spectrum HDAC inhibitors in a physiologically relevant banding model of hypertrophy, observing dose-responsive suppression of ventricular growth that was well tolerated in terms of both clinical outcome and cardiac performance measures. In both short-term (3-week) and long-term (9-week) trials, cardiomyocyte

SUBMITTER: Kong Y 

PROVIDER: S-EPMC4105979 | biostudies-literature | 2006 Jun

REPOSITORIES: biostudies-literature