The role of nitric oxide in atherosclerosis
Abstract
aCooke Pharma, Belmont bDivision of Cardiovascular Medicine, Stanford University, Stanford, California, USA.
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Decreased NO levels contribute to endothelial cell dysfunction, atherosclerotic plaque development, arteriosclerosis, vessel restenosis, peripheral vascular disease, and ischemia-reperfusion injury.
“It is well accepted that decreased NO levels contribute to endothelial cell dysfunction, atherosclerotic plaque development, arteriosclerosis, vessel restenosis, peripheral vascular disease, and ischemia-reperfusion injury [14, 15, 138–140].”
From Inorganic nitrite therapy: historical perspective and future directions (2011) · cites this paper as [138]
Decreased NO levels contribute to endothelial cell dysfunction, atherosclerotic plaque development, arteriosclerosis, vessel restenosis, peripheral vascular disease, and ischemia-reperfusion injury.
“It is well accepted that decreased NO levels contribute to endothelial cell dysfunction, atherosclerotic plaque development, arteriosclerosis, vessel restenosis, peripheral vascular disease, and ischemia-reperfusion injury [14, 15, 138–140].”
From Inorganic nitrite therapy: historical perspective and future directions (2011) · cites this paper as [139]
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“There are multiple mechanisms for impaired endothelial vasodilator function, with one or more mechanisms playing a role in any individual, depending on the associated risk factors and genetic determinants [4].”
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“It thus leads to prevention of the progression of atherosclerosis via its vasodilation, inhibition of VSMC proliferation, platelet adhesion, and LDL oxidation (Maxwell and Cooke, 1999).”
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“A reduction in vascular NO levels has important consequences because of its central role as a vascular protective molecule that retards development of atherosclerosis.(10)”
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“This is likely due to a reduced availability of nitric oxide, possibly associated with an increased formation of reactive oxygen intermediates by macrophages [51, 52].”
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“adhesion, and lipid peroxidation; regulation of insulin and glucose metabolism; and upregulation of antioxidant molecules and enzymes [5,6].”
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“While there is strong functional evidence of NO involvement in native atherosclerosis [27], it is possible thatNOplays a less pivotal role in CAF and, thus, variations in its transcription and structure are of less importance.”
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“We and others have provided evidence that a reduction in the synthesis or bioactivity of endothelium-derived NO promotes processes favoring coronary vascular disease [16–19].”
BackgroundSelf-citationMejía-Montilla, J. (2012) · LA Referencia (Red Federada de Repositorios Institucionales de Publicaciones Científicas)
Espada, C. L. (2005) · Angiología · doi:10.1016/s0003-3170(05)79332-9
(n.d.) · Tesis Doctorals en Xarxa (Consorci de Serveis Universitaris de Catalunya)
- Authors
- Maxwell, A. J., & Cooke, J. P.
- Affiliations
- Stanford Medicine (US)
- Venue
- Coronary Artery Disease
- Published
- 1999
- Volume
- 10
- Issue
- 5
- Pages
- 277-286
- ISSN
- 0954-6928 (ISSN-L)
- OpenAlex
- W1999444674
- Cited by
- 33
- References
- 0
- Citations by year
- 2020: 1 · 2016: 1 · 2014: 1 · 2012: 1
- FWCI
- 2.27
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Coronary Artery Disease (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Health and Disease Prevention
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Keywords
- nitric oxide, atherosclerosis, endothelial function
- MeSH terms
- Arginine, Arteriosclerosis, Coronary Artery Disease, Humans, Nitric Oxide, Risk Factors, Nitric Oxide Synthase
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