Augusto C. Montezano / Augusto CMontezano / Rhian M. Touyz / Rhian MTouyz
Reactive oxygen species (ROS) influence various physiological processes including host defense, hormone biosynthesis, and cellular signaling. Increased ROS production (oxidative stress) is implicated in many diseases of the cardiovascular system, including hypertension, atherosclerosis, cardiac failure, stroke, diabetes, and kidney disease. ROS are produced throughout the cardiovascular system, in the kidney and central and peripheral nervous system. A major source for cardiovascular, renal, and neural ROS is a family of non-phagocytic NAD(P)H oxidases, including the prototypic Nox2 homologue-based NAD(P)H oxidase, as well as other NAD(P)H oxidases, such as Nox1 and Nox4. Other possible sources include mitochondrial electron transport enzymes, xanthine oxidase, cyclooxygenase, lipoxygenase, and uncoupled nitric oxide synthase (NOS). NAD(P)H oxidase-derived ROS is important in regulating endothelial function and vascular tone and oxidative stress is implicated in endothelial dysfunction, inflammation, hypertrophy, apoptosis, migration, fibrosis, angiogenesis and rarefaction, important processes involved in vascular remodeling in cardiovascular disease. These findings have evoked considerable interest because of the possibilities that therapies targeted against non-phagocytic NAD(P)H oxidase to decrease ROS generation and/or strategies to increase nitric oxide (NO) availability and antioxidants may be useful in minimizing vascular injury and thereby prevent or regress target organ damage associated with hypertension and other cardiovascular diseases.
