The DOI matches its Crossref record; 94 of the 94 references it cites were found in a registry or an index.
NAD(P)H Oxidase: Role in Cardiovascular Biology and Disease
Abstract
Abstract —Reactive oxygen species have emerged as important molecules in cardiovascular function. Recent work has shown that NAD(P)H oxidases are major sources of superoxide in vascular cells and myocytes. The biochemical characterization, activation paradigms, structure, and function of this enzyme are now partly understood. Vascular NAD(P)H oxidases share some, but not all, characteristics of the neutrophil enzyme. In response to growth factors and cytokines, they produce superoxide, which is metabolized to hydrogen peroxide, and both of these reactive oxygen species serve as second messengers to activate multiple intracellular signaling pathways. The vascular NAD(P)H oxidases have been found to be essential in the physiological response of vascular cells, including growth, migration, and modification of the extracellular matrix. They have also been linked to hypertension and to pathological states associated with uncontrolled growth and inflammation, such as atherosclerosis.
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“NOXs are multiprotein enzyme complexes that catalyze the electron transfer to molecular oxygen to form ROS, more commonly superoxide, but also hydrogen peroxide (79, 252, 383, 546, 912).”
From Sources of Vascular Nitric Oxide and Reactive Oxygen Species and Their Regulation (2019) · cites this paper as [383]
In the citing paper
“Endothelial cells are a natural source of NO•, and NO• may be generated in mitochondria (137, 139), and with O2•−, to produce ONOO− (and ONOOH), which can modulate cell function”
From Mitochondrial reactive oxygen species production in excitable cells: Modulators of mitochondrial and cell function (2009) · cites this paper as [137]
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“Both enzymes have been implicated as important prooxidant enzymes contributing to hypertension [32,50,51].”
From Sodium nitrite downregulates vascular NADPH oxidase and exerts antihypertensive effects in hypertension (2011) · cites this paper as [51]
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Increased oxidative stress in obesity and its impact on metabolic syndrome
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Metadata
- Authors
- Griendling, K. K., Sorescu, D., & Ushio-Fukai, M.
- Affiliations
- Emory University (US)
- From the Department of Medicine, Division of Cardiology, Emory University, Atlanta, Ga.
- ORCID
- Griendling, Kathy K.
- Venue
- Circulation Research
- Published
- 2000-03-17
- Volume
- 86
- Issue
- 5
- Pages
- 494-501
- ISSN
- 0009-7330 (ISSN-L)
- 1524-4571
- OpenAlex
- W2123799914
- Cited by
- 2,886
- References
- 94
- Citations by year
- 2026: 14 · 2025: 29 · 2024: 27 · 2023: 39 · 2022: 43 · 2021: 62 · 2020: 70 · 2019: 51 · 2018: 64 · 2017: 54 · 2016: 79 · 2015: 79 · 2014: 124 · 2013: 131 · 2012: 137
- FWCI
- 19.54
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Circulation Research (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- National Heart, Lung, and Blood Institute (HL 58000, HL38206, HL58863, P01HL058000, R01HL058863)
- Topics
- Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
- Life Sciences › Immunology and Microbiology › Immunology › Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Keywords
- NADPH oxidase, reactive oxygen species, superoxide, hydrogen peroxide, vascular cells, growth factor signaling, cytokine signaling, intracellular signaling, cell migration, extracellular matrix remodeling, hypertension, atherosclerosis, inflammation
- MeSH terms
- Arteries, Arteriosclerosis, Humans, Myocardium, Reactive Oxygen Species, NADPH Oxidases
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