Role of oxidative stress in atherosclerosis
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.
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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).”
From Sources of Vascular Nitric Oxide and Reactive Oxygen Species and Their Regulation (2019) · cites this paper as [408]
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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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