Cited by 518Nitric Oxide and Endothelin EffectsCardiovascular Health and Disease PreventionAtherosclerosis and Cardiovascular Diseases

Vascular endothelium – Gatekeeper of vessel health

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Cahill, Paul A., Redmond, Eileen M.·2016·Atherosclerosis

Abstract

The vascular endothelium is an interface between the blood stream and the vessel wall. Changes in this single cell layer of the artery wall are believed of primary importance in the pathogenesis of vascular disease/atherosclerosis. The endothelium responds to humoral, neural and especially hemodynamic stimuli and regulates platelet function, inflammatory responses, vascular smooth muscle cell growth and migration, in addition to modulating vascular tone by synthesizing and releasing vasoactive substances. Compromised endothelial function contributes to the pathogenesis of cardiovascular disease; endothelial 'dysfunction' is associated with risk factors, correlates with disease progression, and predicts cardiovascular events. Therapies for atherosclerosis have been developed, therefore, that are directed towards improving endothelial function.

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Crossref · 10.1016/j.atherosclerosis.2016.03.007

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241 of 241 references verified0 citation errors · 0 not checkable

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  • Endothelial cells reconstruct intima structure of vessels and regulate vascular regeneration by secreting VEGF and NO.

    “Endothelial cells can reconstruct the intima structure of vessels and regulate vascular regeneration by secreting growth factors (VEGF) and active factor (NO) [159].”

    From Application of PLCL as a biodegradable polymer in biomedical engineering (2026) · cites this paper as [159]

    The ‘Arterial endothelium: structure, function’ section says endothelial cells form part of the intima, and ‘Endothelial progenitor cells’ says progenitor cells may regenerate an injured endothelial lining. The ‘EDRF/NO’ section confirms that endothelial cells produce and release NO. The paper does not establish that endothelial cells reconstruct the intima and regulate vascular regeneration by secreting both VEGF and NO; its mention of VEGFR2 is a receptor marker, not VEGF secretion. (LLM, conf=0.86)

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Authors
Cahill, P. A., & Redmond, E. M.
Affiliations
  • Dublin City University (IE)
  • University of Rochester Medicine (US)
Corresponding author
Redmond, Eileen M.
Venue
Atherosclerosis
Publisher
Elsevier BV
Published
2016-05
Volume
248
Pages
97-109
ISSN
0021-9150 (ISSN-L)
OpenAlex
W2300272821
Cited by
518
References
241
Citations by year
2026: 23 · 2025: 59 · 2024: 41 · 2023: 50 · 2022: 77 · 2021: 82 · 2020: 62 · 2019: 51 · 2018: 31 · 2017: 31 · 2016: 8 · 2014: 1
FWCI
4.72
Type
journal article
Language
en
Open access
Locations
  • Atherosclerosis (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
National Institute on Alcohol Abuse and Alcoholism (R21AA023213)
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
vascular endothelium, endothelial dysfunction, cardiovascular disease, platelet function, vascular smooth muscle cell migration, vasoactive substances, vascular tone, inflammation
MeSH terms
Animals, Anti-Inflammatory Agents, Cardiovascular Diseases, Coronary Artery Disease, Endothelium, Vascular, Fibrinolytic Agents, Hemodynamics, Humans, Inflammation, Muscle, Smooth, Vascular, Permeability, Risk Factors, Stem Cells, Stress, Mechanical, Vasoconstrictor Agents, Vasodilator Agents, Exercise, Glycocalyx, Atherosclerosis, Mice

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