Cited by 1,275Nitric Oxide and Endothelin EffectsRedox biology and oxidative stressAntioxidant Activity and Oxidative Stress

Role of oxidative stress in atherosclerosis

Harrison, David, Griendling, Kathy K, Landmesser, Ulf, Hornig, Burkhard, Drexler, Helmut·2003·The American Journal of Cardiology

Abstract

The common risk factors for atherosclerosis increase production of reactive oxygen species (ROS) by endothelial, vascular smooth muscle, and adventitial cells. These ROS initiate processes involved in atherogenesis through several important enzyme systems, including xanthine oxidase, nicotinamide adenine dinucleotide phosphate (NADPH) oxidases, and nitric oxide synthase. Physical forces also regulate vascular production of ROS. Oscillatory shear, which is present at sites where atherosclerosis develops, seems a particularly potent stimulus of superoxide production. The signaling cascade for activation of the NAD(P)H oxidase by angiotensin II has recently been elucidated and seems to involve a feed-forward mechanism that permits ongoing production of ROS for prolonged periods. Oxidative stress in humans with coronary artery disease is also exacerbated by a reduction of vascular extracellular superoxide dismutase, normally an important protective enzyme against the superoxide anion.

Integrity signals

Registry

Crossref · 10.1016/s0002-9149(02)03144-2

Cites

21 of 21 references verified0 citation errors · 0 not checkable

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  • Excess superoxide or other ROS in the cell causes modification of different parts of the cellular machinery and is a known player in the genesis and progression of cardiovascular disease.

    “The excess of superoxide, or other ROS, in the cell causes the modification of different parts of the cellular machinery and is a known player in the genesis and progression of cardiovascular disease (227, 408, 409, 570, 672, 700, 893).”

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Authors
Harrison, D., Griendling, K. K., Landmesser, U., Hornig, B., & Drexler, H.
Affiliations
  • Emory University (US)
  • Medizinische Hochschule Hannover (DE)
Corresponding author
Harrison, David
Venue
The American Journal of Cardiology
Publisher
Elsevier BV
Published
2003-02
Volume
91
Issue
3
Pages
7-11
ISSN
0002-9149 (ISSN-L)
OpenAlex
W2059571803
Cited by
1,275
References
21
Citations by year
2026: 17 · 2025: 19 · 2024: 23 · 2023: 34 · 2022: 53 · 2021: 48 · 2020: 66 · 2019: 52 · 2018: 62 · 2017: 61 · 2016: 60 · 2015: 62 · 2014: 54 · 2013: 74 · 2012: 72
FWCI
35.26
Type
journal article
Language
en
Open access
closed
Locations
  • The American Journal of Cardiology (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
  • Health Sciences › Medicine › Biochemistry › Antioxidant Activity and Oxidative Stress
Keywords
oxidative stress, atherosclerosis, reactive oxygen species, atherogenesis, xanthine oxidase, NADPH oxidase, nitric oxide synthase, oscillatory shear, superoxide production, angiotensin II signaling, extracellular superoxide dismutase, coronary artery disease, vascular smooth muscle cells, endothelial cells
MeSH terms
Arteriosclerosis, Humans, Risk Factors, Signal Transduction, Oxidative Stress

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