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Cited by 586Renin-Angiotensin System StudiesAtherosclerosis and Cardiovascular DiseasesNitric Oxide and Endothelin Effects

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Vascular Inflammation and the Renin-Angiotensin System

Brasier, Allan R., Recinos, Adrian, Eledrisi, Mohsen S.·2002·Arteriosclerosis, Thrombosis, and Vascular Biology
DOI 10.1161/01.atv.0000021412.56621.a2
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Abstract

It is now well established that vascular inflammation is an independent risk factor for the development of atherosclerosis. In otherwise healthy patients, chronic elevations of circulating interleukin-6 or its biomarkers are predictors for increased risk in the development and progression of ischemic heart disease. Although multifactorial in etiology, vascular inflammation produces atherosclerosis by the continuous recruitment of circulating monocytes into the vessel wall and by contributing to an oxidant-rich inflammatory milieu that induces phenotypic changes in resident (noninflammatory) cells. In addition, the renin-angiotensin system (RAS) has important modulatory activities in the atherogenic process. Recent work has shown that angiotensin II (Ang II) has significant proinflammatory actions in the vascular wall, inducing the production of reactive oxygen species, inflammatory cytokines, and adhesion molecules. These latter effects on gene expression are mediated, at least in part, through the cytoplasmic nuclear factor-kappaB transcription factor. Through these actions, Ang II augments vascular inflammation, induces endothelial dysfunction, and, in so doing, enhances the atherogenic process. Our recent studies have defined a molecular mechanism for a biological positive-feedback loop that explains how vascular inflammation can be self-sustaining through upregulation of the vessel wall Ang II tone. Ang II produced locally by the inflamed vessel induces the synthesis and…

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Metadata

Authors
Brasier, A. R., Recinos, A., & Eledrisi, M. S.
Affiliations
  • The University of Texas Medical Branch at Galveston (US)
  • From the Departments of Medicine (A.R.B., A.R., M.S.E.) and Human Biological Chemistry and Genetics (A.R.B.) and the Sealy Center for Molecular Sciences (A.R.B.), The University of Texas Medical Branch, Galveston.
ORCID
Venue
Arteriosclerosis, Thrombosis, and Vascular Biology
Publisher
Ovid Technologies (Wolters Kluwer Health)
Published
2002-08
Volume
22
Issue
8
Pages
1257-1266
ISSN
  • 1079-5642 (ISSN-L)
  • 1524-4636
DOI
10.1161/01.atv.0000021412.56621.a2
OpenAlex
W2154360613
Cited by
586
References
126
Citations by year
2026: 4 · 2025: 17 · 2024: 12 · 2023: 16 · 2022: 9 · 2021: 20 · 2020: 21 · 2019: 12 · 2018: 16 · 2017: 22 · 2016: 24 · 2015: 22 · 2014: 25 · 2013: 22 · 2012: 29
FWCI
5.16
Type
journal article
Language
en
Open access
closed
Locations
  • Arteriosclerosis Thrombosis and Vascular Biology (publishedVersion)
  • PubMed (publishedVersion)
Funders
U.S. Public Health Service (55630)
Topics
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Renin-Angiotensin System Studies
  • Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
  • Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
Keywords
vascular inflammation, renin-angiotensin system, angiotensin II, atherosclerosis, interleukin-6, nuclear factor-kappaB, JAK/STAT3 signaling, angiotensinogen, oxidized lipids, endothelial dysfunction, monocyte recruitment, reactive oxygen species, ischemic heart disease
MeSH terms
Acute-Phase Proteins, Angiotensin II, Animals, Arteriosclerosis, Endothelium, Vascular, Humans, Inflammation, Cholesterol, LDL, Liver, Macrophages, Monocytes, Oxidation-Reduction, Renin-Angiotensin System, Signal Transduction, Interleukin-6, Reactive Oxygen Species, Feedback, Physiological

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