Changes in cardiac Nav1.5 expression, function, and acetylation by pan-histone deacetylase inhibitors

Therapeutic histone deacetylase inhibition with vorinostat or romidepsin significantly reduces ventricular sodium current density and NaV1.5 protein expression. A slight positive shift in the voltage activation curve, presumably the result of lysine acetylation, decreases the inactivation rate at low activating potentials but does not increase the late sodium current amplitude.