Reactive oxygen species (ROS) function as regulators of cell growth, adhesion, differentiation, migration, senescence, and
apoptosis, but given their highly reactive free-radical nature, ROS levels must be tightly regulated. Pathological conditions
that are associated with ROS are fairly common, typified by endothelial dysfunction, vascular reactivity, arterial remodeling,
and vascular inflammation. Cardiovascular ROS are primarily generated by distinct members of the NADPH oxidase (NOX) family
of enzymes. The regulation of NOX activity is mediated through multiple protein interactions, many of which are just beginning
to be elucidated, but it is clear that each of the four important cardiovascular NOX isoforms manifests distinct sets of protein
interactions. The design of novel therapeutics that may exploit the growing array of NOX regulatory mechanisms is an important
line of antioxidant research.
