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

Vascular inflammation and the renin-angiotensin system

Brasier, Allan R., Recinos, Adrian, Eledrisi, Mohsen S.·2002·Arteriosclerosis, Thrombosis, and Vascular Biology

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…

Integrity signals

Registry

Crossref · 10.1161/01.atv.0000021412.56621.a2

Cites

126 of 126 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • The AngII-AT1R axis activates the NF-κB pathway through various growth factors and pro-inflammatory cytokines.

    “The AngII–AT1R axis activates the NF-κB pathway through various growth factors and pro-inflammatory cytokines (347, 348).”

    From IL-6 in inflammation, autoimmunity and cancer (2021) · cites this paper as [347]

Cites

Flagged first, then by citations

Cited by

Sorted by citations

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.
Venue
Arteriosclerosis, Thrombosis, and Vascular Biology
Published
2002-08
Volume
22
Issue
8
Pages
1257-1266
ISSN
  • 1079-5642 (ISSN-L)
  • 1524-4636
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 › 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

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review