Background: Generation of reactive oxygen species (ROS) plays a pivotal role in the progression of heart failure. Primary endogenous sources of H2O2 und O2·− are tightly regulated NADPH oxidases (NOX), modulating redox-sensitive effector proteins. While exerting distinct physiological functions in tissue homeostasis, enhanced ROS activity, as well as upregulation of NOX expression has been identified to have detrimental effects in the progression of heart failure.