The DOI matches its Crossref record; 584 of the 584 references it cites were found in a registry or an index.
Redox Control of Endothelial Function and Dysfunction: Molecular Mechanisms and Therapeutic Opportunities
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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“Indeed, elevated ROS levels lead to endothelial dysfunction171, an early event in atherosclerosis pathogenesis that occurs mainly in atherosclerotic lesion formation172,173.”
From Mitochondrial and metabolic dysfunction in ageing and age-related diseases (2022) · cites this paper as [171]
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3 retracted
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RetractedAbid, M. R., Tsai, J. C., Spokes, K., Deshpande, S. S., Irani, K., & Aird, W. C. (2001) · The FASEB Journal · doi:10.1096/fj.01-0338fje · Cited by 157
RetractedUncoupling of Endothelial Nitric Oxidase Synthase by Hypochlorous Acid
Xu, J., Xie, Z., Reece, R., Pimental, D. R., & Zou, M. (2006) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/01.atv.0000249394.94588.82 · Cited by 146
RetractedThe NOX Family of ROS-Generating NADPH Oxidases: Physiology and Pathophysiology
Bedard, K., & Krause, K.-H. (2007) · Physiological Reviews · doi:10.1152/physrev.00044.2005 · Cited by 6,989
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Normalizing mitochondrial superoxide production blocks three pathways of hyperglycaemic damage
Nishikawa, T., Edelstein, D., Du, X. L., Yamagishi, S.-I., Matsumura, T., Kaneda, Y., Yorek, M. A., Beebe, D., Oates, P. J., Hammes, H.-P., et al. (2000) · Nature · doi:10.1038/35008121 · Cited by 4,277
Endothelial dysfunction in cardiovascular diseases: the role of oxidant stress
Cai, H., & Harrison, D. G. (2000) · Circulation Research · doi:10.1161/01.res.87.10.840 · Cited by 3,839
Circulating endothelial progenitor cells, vascular function, and cardiovascular risk
Hill, J. M., Zalos, G., Halcox, J. P. J., Schenke, W. H., Waclawiw, M. A., Quyyumi, A. A., & Finkel, T. (2003) · New England Journal of Medicine · doi:10.1056/nejmoa022287 · Cited by 3,423
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Incalza, M. A., D’Oria, R., Natalicchio, A., Perrini, S., Laviola, L., & Giorgino, F. (2017) · Vascular Pharmacology · doi:10.1016/j.vph.2017.05.005 · Cited by 1,419
Coronary Microvascular Dysfunction
Crea, F., Lanza, G. A., & Camici, P. G. (2013) · Springer eBooks · doi:10.1007/978-88-470-5367-0 · Cited by 1,295
Mitochondrial and metabolic dysfunction in ageing and age-related diseases
Amorim, J. A., Coppotelli, G., Rolo, A. P., Palmeira, C. M., Ross, J. M., & Sinclair, D. A. (2022) · Nature Reviews Endocrinology · doi:10.1038/s41574-021-00626-7 · Cited by 990
Combating oxidative stress in vascular disease: NADPH oxidases as therapeutic targets
Drummond, G. R., Selemidis, S., Griendling, K. K., & Sobey, C. G. (2011) · Nature Reviews Drug Discovery · doi:10.1038/nrd3403 · Cited by 899
Self-citationReactive oxygen species, heat stress and oxidative-induced mitochondrial damage. A review
Slimen, I. B., Najar, T., Ghram, A., Debbabi, H., Mrad, M. B., & Abderrabba, M. (2014) · International Journal of Hyperthermia · doi:10.3109/02656736.2014.971446 · Cited by 905
Metadata
- Authors
- Thomas, S. R., Witting, P. K., & Drummond, G. R.
- Affiliations
- UNSW Sydney (AU)
- Concord Repatriation General Hospital (AU)
- Monash University (AU)
- Venue
- Antioxidants & Redox Signaling
- Publisher
- SAGE Publications
- Published
- 2008-10
- Volume
- 10
- Issue
- 10
- Pages
- 1713-1766
- ISSN
- 1523-0864 (ISSN-L)
- 1557-7716
- 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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