Postnatal cardiac myocytes respond to stress signals by hypertrophic growth and activation
of a fetal gene program. Recently, we showed that class II histone deacetylases (HDACs)
suppress cardiac hypertrophy, and mice lacking the class II HDAC, HDAC9, are sensitized to
hypertrophic signals. To further define the roles of HDACs in cardiac hypertrophy, we
analyzed the effects of HDAC inhibitors on the responsiveness of primary cardiomyocytes to
hypertrophic agonists. Paradoxically, HDAC inhibitors imposed a dose-dependent blockade …