Abstract
Oxidative stress, resulting from increased production of reactive oxygen species (ROS) and/or reduced antioxidant defences, has been implicated in cardiovascular disease pathophysiology for over 2 decades. Based on the concept that this drives both the genesis and progression of conditions such as heart failure, numerous clinical trials of antioxidant therapies were undertaken but were unsuccessful. Nevertheless, experimental data linking oxidative stress and heart disease remain compelling and support continued efforts to develop more effective therapies than antioxidant vitamins.1 In the current issue of Circulation , Zhao et al .2 report that cardiomyocyte-specific high-level overexpression of the ROS-generating enzyme NADPH oxidase-4 (Nox4) aggravated angiotensin II-induced cardiac remodeling and was mitigated by a small molecule Nox inhibitor. The authors propose that Nox4 inhibition may have therapeutic potential to treat cardiac remodeling. Is this proposal reasonable and how should such studies be interpreted within a pathophysiological framework for the roles of ROS in heart failure?
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