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NADPH Oxidases, Reactive Oxygen Species, and Hypertension
Open accessAbstract
Reactive oxygen species (ROS) influence many physiological processes including host defense, hormone biosynthesis, fertilization, and cellular signaling. Increased ROS production (termed “oxidative stress”) has been implicated in various pathologies, including hypertension, atherosclerosis, diabetes, and chronic kidney disease. A major source for vascular and renal ROS is a family of nonphagocytic NAD(P)H oxidases, including the prototypic Nox2 homolog-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. NAD(P)H oxidase-derived ROS plays a physiological role in the regulation of endothelial function and vascular tone and a pathophysiological role in endothelial dysfunction, inflammation, hypertrophy, apoptosis, migration, fibrosis, angiogenesis, and rarefaction, important processes underlying cardiovascular and renal remodeling in hypertension and diabetes. These findings have evoked considerable interest because of the possibilities that therapies against nonphagocytic 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 renal dysfunction and thereby prevent or regress target organ damage associated with hypertension and diabetes. Here we highlight current developments in the field of reactive oxygen species and cardiovascular disease, focusing specifically on the recently identified novel Nox family of NAD(P)H oxidases in hypertension. We also discuss the potential role of targeting ROS as a therapeutic possibility in the management of hypertension and cardiovascular disease.
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Self-citation
Cited by
Consequences of oxidative stress in age-related macular degeneration
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Renal Autoregulation in Health and Disease
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Endothelial Dysfunction: Is There a Hyperglycemia-Induced Imbalance of NOX and NOS?
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Health Effects with Consumption of the Flax Lignan Secoisolariciresinol Diglucoside
Adolphe, J. L., Whiting, S. J., Juurlink, B. H. J., Thorpe, L. U., & Alcorn, J. (2010) · British Journal of Nutrition · doi:10.1017/s0007114509992753 · Cited by 314
Metadata
- Authors
- Paravicini, T. M., & Touyz, R. M.
- Venue
- Diabetes Care
- Publisher
- American Diabetes Association
- Published
- 2008-02-01
- Volume
- 31
- Issue
- Supplement_2
- Pages
- S170-S180
- ISSN
- 0149-5992 (ISSN-L)
- 1935-5548
- OpenAlex
- W2078593792
- Cited by
- 724
- References
- 18
- FWCI
- 33.78
- Type
- journal article
- Language
- en
- Open access
- bronze
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