Cited by 1,618Nitric Oxide and Endothelin EffectsAntioxidant Activity and Oxidative StressRedox biology and oxidative stress

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Oxidative Stress and Vascular Disease

Madamanchi, Nageswara R., Vendrov, Aleksandr, Runge, Marschall S.·2005·Arteriosclerosis, Thrombosis, and Vascular Biology

DOI 10.1161/01.atv.0000150649.39934.13

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Abstract

Growing evidence indicates that chronic and acute overproduction of reactive oxygen species (ROS) under pathophysiologic conditions is integral in the development of cardiovascular diseases (CVD). These ROS can be released from nicotinamide adenine dinucleotide (phosphate) oxidase, xanthine oxidase, lipoxygenase, mitochondria, or the uncoupling of nitric oxide synthase in vascular cells. ROS mediate various signaling pathways that underlie vascular inflammation in atherogenesis: from the initiation of fatty streak development through lesion progress to ultimate plaque rupture. Various animal models of oxidative stress support the notion that ROS have a causal role in atherosclerosis and other cardiovascular diseases. Human investigations also support the oxidative stress hypothesis of atherosclerosis. Oxidative stress is the unifying mechanism for many CVD risk factors, which additionally supports its central role in CVD. Despite the demonstrated role of antioxidants in cellular and animal studies, the ineffectiveness of antioxidants in reducing cardiovascular death and morbidity in clinical trials has led many investigators to question the importance of oxidative stress in human atherosclerosis. Others have argued that the prime factor for the mixed outcomes from using antioxidants to prevent CVD may be the lack of specific and sensitive biomarkers by which to assess the oxidative stress phenotypes underlying CVD. A better understanding of the complexity of cellular redox reactions, development of a new class of antioxidants targeted to specific subcellular locales, and the phenotype-genotype linkage analysis for oxidative stress will likely be avenues for future research in this area as we move toward the broader use of pharmacological and regenerative therapies in the treatment and prevention of CVD.

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Background

Authors: Madamanchi, N. R., Vendrov, A., & Runge, M. S.
Affiliations: University of North Carolina at Chapel Hill (US)
ORCID: Madamanchi, Nageswara R.
Vendrov, Aleksandr
Runge, Marschall S.
Venue: Arteriosclerosis, Thrombosis, and Vascular Biology
Publisher: Ovid Technologies (Wolters Kluwer Health)
Published: 2005-01
Volume: 25
Issue: 1
Pages: 29-38
ISSN: 1079-5642 (ISSN-L)
1524-4636
DOI: 10.1161/01.atv.0000150649.39934.13
OpenAlex: W2109698138
Cited by: 1,618
References: 135
Citations by year: 2026: 47 · 2025: 46 · 2024: 42 · 2023: 53 · 2022: 61 · 2021: 62 · 2020: 73 · 2019: 73 · 2018: 57 · 2017: 75 · 2016: 78 · 2015: 105 · 2014: 111 · 2013: 104 · 2012: 95
FWCI: 7.02
Type: journal article
Language: en
Open access: closed
Locations: Arteriosclerosis Thrombosis and Vascular Biology (publishedVersion)
PubMed (publishedVersion)
Topics: Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
Health Sciences › Medicine › Biochemistry (medical) › Antioxidant Activity and Oxidative Stress
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
Keywords: oxidative stress, reactive oxygen species, atherosclerosis, vascular disease, cardiovascular disease, NADPH oxidase, xanthine oxidase, lipoxygenase, nitric oxide synthase uncoupling, vascular inflammation, atherogenesis, antioxidants, redox signaling, biomarkers, cardiovascular risk factors
MeSH terms: Animals, Humans, Vascular Diseases, Oxidative Stress

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