Inhibition of histone deacetylase reduces transcription of NADPH oxidases and ROS production and ameliorates pulmonary arterial hypertension.

ABSTRACT: Excessive levels of reactive oxygen species (ROS) and increased expression of NADPH oxidases (Nox) have been proposed to contribute to pulmonary artery hypertension (PAH) and other cardiovascular diseases (CVD). Nox enzymes are major sources of ROS but the mechanisms regulating changes in Nox expression in disease states remain poorly understood. Epigenetics encompasses a number of mechanisms that cells employ to regulate the ability to read and transcribe DNA. Histone acetylation is a prominent example of an epigenetic mechanism regulating the expression of numerous genes by altering chromatin accessibility. The goal of this study was to determine whether inhibition of histone deacetylases (HDAC) affects the expression of Nox isoforms and reduces pulmonary hypertension. In immune cells, w

SUBMITTER: Chen F 

PROVIDER: S-EPMC5240036 | biostudies-literature | 2016 Oct

REPOSITORIES: biostudies-literature