Cited by 383Nitric Oxide and Endothelin EffectsRedox biology and oxidative stressCardiovascular Health and Disease Prevention

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Redox Control of Endothelial Function and Dysfunction: Molecular Mechanisms and Therapeutic Opportunities

Thomas, Shane R., Witting, Paul K., Drummond, Grant R.·2008·Antioxidants & Redox Signaling

DOI 10.1089/ars.2008.2027

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Abstract

The endothelium is essential for the maintenance of vascular homeostasis. Central to this role is the production of endothelium-derived nitric oxide (EDNO), synthesized by the endothelial isoform of nitric oxide synthase (eNOS). Endothelial dysfunction, manifested as impaired EDNO bioactivity, is an important early event in the development of various vascular diseases, including hypertension, diabetes, and atherosclerosis. The degree of impairment of EDNO bioactivity is a determinant of future vascular complications. Accordingly, growing interest exists in defining the pathologic mechanisms involved. Considerable evidence supports a causal role for the enhanced production of reactive oxygen species (ROS) by vascular cells. ROS directly inactivate EDNO, act as cell-signaling molecules, and promote protein dysfunction, events that contribute to the initiation and progression of endothelial dysfunction. Increasing data indicate that strategies designed to limit vascular ROS production can restore endothelial function in humans with vascular complications. The purpose of this review is to outline the various ways in which ROS can influence endothelial function and dysfunction, describe the redox mechanisms involved, and discuss approaches for preventing endothelial dysfunction that may highlight future therapeutic opportunities in the treatment of cardiovascular disease.

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See all 383

Authors: Thomas, S. R., Witting, P. K., & Drummond, G. R.
Affiliations: UNSW Sydney (AU)
Concord Repatriation General Hospital (AU)
Monash University (AU)
ORCID: Thomas, Shane R.
Witting, Paul K.
Drummond, Grant R.
Venue: Antioxidants & Redox Signaling
Publisher: SAGE Publications
Published: 2008-10
Volume: 10
Issue: 10
Pages: 1713-1766
ISSN: 1523-0864 (ISSN-L)
1557-7716
DOI: 10.1089/ars.2008.2027
OpenAlex: W2014374142
Cited by: 383
References: 577
Citations by year: 2026: 7 · 2025: 7 · 2024: 9 · 2023: 7 · 2022: 18 · 2021: 12 · 2020: 20 · 2019: 13 · 2018: 13 · 2017: 24 · 2016: 23 · 2015: 17 · 2014: 38 · 2013: 22 · 2012: 42
FWCI: 4.00
Type: journal article
Language: en
Open access: closed
Locations: Antioxidants and Redox Signaling (publishedVersion)
PubMed (publishedVersion)
Topics: Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Health and Disease Prevention
Keywords: endothelial dysfunction, endothelial function, reactive oxygen species, nitric oxide, endothelial nitric oxide synthase, redox signaling, vascular homeostasis, hypertension, diabetes mellitus, atherosclerosis, cardiovascular disease, antioxidant therapy
MeSH terms: Angiotensin-Converting Enzyme Inhibitors, Animals, Antioxidants, Endothelium, Vascular, Humans, Hydrogen Peroxide, Mitochondria, Nitric Oxide, Oxidation-Reduction, Oxidoreductases, Phosphoric Monoester Hydrolases, Protein Kinases, Superoxides, Thioredoxins, Transcription Factors, Vascular Diseases, Lipid Peroxidation, Oxidative Stress, Hydroxymethylglutaryl-CoA Reductase Inhibitors, Endothelial Cells, Nitric Oxide Synthase Type III

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Redox Control of Endothelial Function and Dysfunction: Molecular Mechanisms and Therapeutic Opportunities

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