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NOX1, 2, 4, 5: counting out oxidative stress
Open accessAbstract
For decades, oxidative stress has been discussed as a key mechanism of endothelial dysfunction and cardiovascular disease. However, attempts to validate and exploit this hypothesis clinically by supplementing antioxidants have failed. Nevertheless, this does not disprove the oxidative stress hypothesis. As a certain degree of reactive oxygen species (ROS) formation appears to be physiological and beneficial. To reduce oxidative stress therapeutically, two alternative approaches are being developed. One is the repair of key signalling components that are compromised by oxidative stress. These include uncoupled endothelial nitric oxide (NO) synthase and oxidized/heme‐free NO receptor soluble guanylate cyclase. A second approach is to identify and effectively inhibit the relevant source(s) of ROS in a given disease condition. A highly likely target in this context is the family of NADPH oxidases. Animal models, including NOX knockout mice and new pharmacological inhibitors of NADPH oxidases have opened up a new era of oxidative stress research and have paved the way for new cardiovascular therapies. LINKED ARTICLES This article is part of a themed issue on Vascular Endothelium in Health and Disease. To view the other articles in this issue visit http://dx.doi.org/10.1111/bph.2011.164.issue‐3
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“Instead, apocynin directly scavenges ROS due to its antioxidant capacities [340,395,396,397,398].”
From Functions of ROS in Macrophages and Antimicrobial Immunity (2021) · cites this paper as [340]
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“Apocynin was long considered as specific Nox2 inhibitor. However, several studies have shown that this is indeed not the case.”
From Functions of ROS in Macrophages and Antimicrobial Immunity (2021) · cites this paper as [340]
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Self-citation
Metadata
- Authors
- Wingler, K., Hermans, J., Schiffers, P., Moens, A., Paul, M., & Schmidt, H.
- Affiliations
- Maastricht University (NL)
- Maastricht University Medical Centre (NL)
- ORCID
- Venue
- British Journal of Pharmacology
- Publisher
- Wiley
- Published
- 2011-09-08
- Volume
- 164
- Issue
- 3
- Pages
- 866-883
- ISSN
- 0007-1188 (ISSN-L)
- 1476-5381
- PMC
- PMC3195911
- OpenAlex
- W1512037315
- Cited by
- 113
- References
- 176
- Citations by year
- 2026: 1 · 2025: 3 · 2024: 4 · 2023: 2 · 2022: 7 · 2021: 8 · 2020: 9 · 2019: 6 · 2018: 8 · 2017: 5 · 2016: 7 · 2015: 8 · 2014: 12 · 2013: 15 · 2012: 15
- FWCI
- 1.54
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- British Journal of Pharmacology (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Research Publications (Maastricht University) (publishedVersion, other-oa)
- Research Publications (Maastricht University) (submittedVersion, other-oa)
- Funders
- ZonMw
- Nederlandse Organisatie voor Wetenschappelijk Onderzoek
- Servier
- Medical Research Council
- National Health and Medical Research Council
- 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
- Life Sciences › Immunology and Microbiology › Immunology › Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Keywords
- oxidative stress, NADPH oxidase, NOX1, NOX2, NOX4, NADPH oxidase 5, reactive oxygen species, endothelial dysfunction, cardiovascular disease, antioxidant supplementation, soluble guanylate cyclase, NADPH oxidase inhibitors
- MeSH terms
- Animals, Cardiovascular Agents, Cardiovascular Diseases, Humans, Oxidative Stress, NADPH Oxidases
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