The DOI matches its Crossref record; 48 of the 48 references it cites were found in a registry or an index.
Endothelial Dysfunction in Cardiovascular Diseases: The Role of Oxidant Stress
Abstract
Accumulating evidence suggests that oxidant stress alters many functions of the endothelium, including modulation of vasomotor tone. Inactivation of nitric oxide (NO(.)) by superoxide and other reactive oxygen species (ROS) seems to occur in conditions such as hypertension, hypercholesterolemia, diabetes, and cigarette smoking. Loss of NO(.) associated with these traditional risk factors may in part explain why they predispose to atherosclerosis. Among many enzymatic systems that are capable of producing ROS, xanthine oxidase, NADH/NADPH oxidase, and uncoupled endothelial nitric oxide synthase have been extensively studied in vascular cells. As the role of these various enzyme sources of ROS become clear, it will perhaps be possible to use more specific therapies to prevent their production and ultimately correct endothelial dysfunction.
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“Xdh-derived ROS are proinflammatory in the vasculature as they increase vascular permeability and arteriolar tone [57] and thus promote hypertension, cardiovascular diseases, and atherosclerosis [58,59].”
From Genetic variation in CCDC93 is associated with elevated central systolic blood pressure, impaired arterial relaxation, and mitochondrial dysfunction (2024) · cites this paper as [57]
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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 [50]
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Cites
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- 10.1161/res.69.5.1934359 · DOI
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Metadata
- Authors
- Cai, H., & Harrison, D. G.
- Affiliations
- Emory University (US)
- Venue
- Circulation Research
- Published
- 2000-11-10
- Volume
- 87
- Issue
- 10
- Pages
- 840-844
- ISSN
- 0009-7330 (ISSN-L)
- 1524-4571
- OpenAlex
- W2148637873
- Cited by
- 3,839
- References
- 48
- Citations by year
- 2026: 61 · 2025: 66 · 2024: 84 · 2023: 99 · 2022: 114 · 2021: 115 · 2020: 125 · 2019: 136 · 2018: 143 · 2017: 167 · 2016: 163 · 2015: 171 · 2014: 197 · 2013: 195 · 2012: 208
- FWCI
- 13.63
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Circulation Research (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (HL39006, HL58000)
- National Heart, Lung, and Blood Institute (HL59243, HL 58000, R01HL039006, R01HL39006, P01HL058000)
- Topics
- Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Health and Disease Prevention
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Keywords
- endothelial dysfunction, oxidative stress, reactive oxygen species, nitric oxide, superoxide, xanthine oxidase, NADPH oxidase, uncoupled nitric oxide synthase, hypertension, hypercholesterolemia, diabetes mellitus, cigarette smoking, atherosclerosis, vascular tone
- MeSH terms
- Animals, Cardiovascular Diseases, Endothelium, Vascular, Humans, NADH, NADPH Oxidoreductases, Nitric Oxide, Xanthine Oxidase, Reactive Oxygen Species, Oxidative Stress, Nitric Oxide Synthase, Nitric Oxide Synthase Type III
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