Cited by 114Nitric Oxide and Endothelin EffectsRedox biology and oxidative stressNeutrophil, Myeloperoxidase and Oxidative Mechanisms

Nox1, 2, 4, 5: Counting out oxidative stress

Open access
Wingler, K, Hermans, JJR, Schiffers, P, Moens, AL, Paul, M, Schmidt, HHHW·2011·British Journal of Pharmacology

Abstract

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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Crossref · 10.1111/j.1476-5381.2011.01249.x

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  • Apocynin directly scavenges ROS due to its antioxidant capacities.

    “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]

  • Apocynin was long considered as a specific Nox2 inhibitor, but several studies have shown that this is not the case.

    “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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Authors
Wingler, K., Hermans, J., Schiffers, P., Moens, A., Paul, M., & Schmidt, H.
Affiliations
  • Maastricht University (NL)
  • Maastricht University Medical Centre (NL)
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
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
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 › 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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