Abstract
Objective: Reactive oxygen species (ROS) have been implicated in the progression of ventricular hypertrophy to congestive heart failure. However, the source of increased oxidative stress in cardiomyocytes remains unclear. Methods: Here we examined NADPH oxidase and mitochondria as sources of ventricular ROS production in a rat model of right-ventricular (RV) failure (CHF) induced by pulmonary arterial hypertension (PAH). Results: Western analysis showed increased expression of the catalytic subunit gp91
Original language | English |
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Pages (from-to) | 770-781 |
Journal | Cardiovascular Research |
Volume | 74 |
DOIs | |
Publication status | Published - 2007 |