Flow, NO, and atherogenesis
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Proceedings of the National Academy of Sciences (PNAS), a peer reviewed journal of the National Academy of Sciences (NAS) - an authoritative source of high-impact, original research that broadly spans the biological, physical, and social sciences.
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Endothelium-derived NO suppresses endothelial expression of adhesion molecules and chemokines that would otherwise initiate vascular inflammation.
“Finally, endotheliumderived NO suppresses the endothelial expression of adhesion molecules and chemokines that would otherwise initiate vascular inflammation (3).”
From Dietary nitrate, nitric oxide, and restenosis (2011) · cites this paper as [3]
Endothelium-derived NO suppresses platelet adhesion, leukocyte infiltration, and VSMC proliferation and migration.
“Endothelium-derived NO suppresses platelet adhesion, leukocyte infiltration, and VSMC proliferation and migration (3).”
From Dietary nitrate, nitric oxide, and restenosis (2011) · cites this paper as [3]
Endothelium-derived NO controls the contractility and growth state of the underlying vascular smooth muscle cells and regulates the interaction of the vessel wall with circulating blood elements.
“Endothelium-derived NO controls the contractility and growth state of the underlying vascular smooth muscle cells and regulates the interaction of the vessel wall with circulating blood elements.”
From Dietary nitrate, nitric oxide, and restenosis (2011) · cites this paper as [3]
Endothelial synthesis of NO is highly regulated in response to hemodynamic and humoral factors.
“The endothelial synthesis of this potent molecule is highly regulated, in response to hemodynamic (e.g., shear stress) as well as humoral (e.g., serotonin) factors (3).”
From Dietary nitrate, nitric oxide, and restenosis (2011) · cites this paper as [3]
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- Authors
- Cooke, J. P.
- Affiliations
- Stanford Medicine (US)
- Corresponding author
- Cooke, John P.
- ORCID
- Cooke, John P.
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2003-01-27
- Volume
- 100
- Issue
- 3
- Pages
- 768-770
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC298674
- OpenAlex
- W2039110457
- Cited by
- 135
- References
- 40
- Citations by year
- 2026: 3 · 2024: 2 · 2023: 4 · 2022: 2 · 2021: 9 · 2020: 6 · 2019: 4 · 2018: 3 · 2017: 5 · 2016: 7 · 2015: 6 · 2014: 9 · 2013: 7 · 2012: 14
- FWCI
- 1.11
- Type
- journal article
- Language
- en
- Update notices
- correction (2004-12-28)
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (1z01hl000204-29)
- National Institute on Aging (P01 AG18784, P01AG018784)
- National Heart, Lung, and Blood Institute (R01 HL-63685, R01 HL-75774, R01HL075774, R01HL063685)
- National Institute of Allergy and Infectious Diseases (P01AI050153, P01AI50153)
- National Center for Complementary and Integrative Health (R01 AT/HL00204)
- Topics
- Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Health and Disease Prevention
- Keywords
- nitric oxide, atherogenesis, blood flow, atherosclerosis
- MeSH terms
- Animals, Arteriosclerosis, Blood Flow Velocity, Cardiovascular Diseases, Endothelium, Vascular, Humans, Models, Biological, Nitric Oxide, Oxidative Stress, Nitric Oxide Synthase
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