NADPH oxidases (NOXs) represent one of the major sources of reactive oxygen species in the vascular district. Reactive oxygen species are responsible for vascular damage that leads to several cardiovascular pathological conditions. Among NOX isoforms, NOX2 is widely expressed in many cells types, such as cardiomyocytes, endothelial cells, and vascular smooth muscle cells, confirming its pivotal role in vascular pathophysiology. Studies in mice models with systemic deletion of NOX2, as well as in transgenic mice overexpressing NOX2, have demonstrated the undeniable involvement of NOX2 in the development of hypertension, atherosclerosis, diabetes mellitus, cardiac hypertrophy, platelet aggregation, and aging. Of note, the inhibition of NOX2 has been found to be protective for cardiovascular homeostasis. Here, we review the evidence demonstrating that the modulation of NOX2 activity is able to improve vascular physiology, suggesting that NOX2 may be a potential target for therapeutic applications.
Keywords: Cardiac hypertrophy; Hypertension; NADPH oxidase; NOX2; Reactive oxygen species.