NADPH oxidase 4 protects against development of endothelial dysfunction and atherosclerosis in LDL receptor deficient mice
Open accessAbstract
AIMS: Endothelial dysfunction is an early step in the development of atherosclerosis. Increased formation of superoxide anions by NADPH oxidase Nox1, 2, and 5 reduces nitric oxide availability and can promote endothelial dysfunction. In contrast, recent evidence supports a vasoprotective role of H2O2 produced by main endothelial isoform Nox4. Therefore, we analysed the impact of genetic deletion of Nox4 on endothelial dysfunction and atherosclerosis in the low-density lipoprotein receptor (Ldlr) knockout model. METHODS AND RESULTS: Ex vivo analysis of endothelial function by Mulvany myograph showed impaired endothelial function in thoracic aorta of Nox4(-/-)/Ldlr(-/-) mice. Further progression of endothelial dysfunction due to high-fat diet increased atherosclerotic plaque burden and galectin-3 staining in Nox4(-/-)/Ldlr(-/-) mice compared with Ldlr(-/-) mice. Under physiological conditions, loss of Nox4 does not influence aortic vascular function. In this setting, loss of Nox4-derived H2O2 production could be partially compensated for by nNOS upregulation. Using an innovative optical coherence tomography approach, we were able to analyse endothelial function by flow-mediated vasodilation in the murine saphenous artery in vivo. This new approach revealed an altered flow-mediated dilation in Nox4(-/-) mice, indicating a role for Nox4 under physiological conditions in peripheral arteries in vivo. CONCLUSIONS: Nox4 plays an important role in maintaining endothelial function under physiological and pathological conditions. Loss of Nox4-derived H2O2 could be partially compensated for by nNOS upregulation, but severe endothelial dysfunction is not reversible. This leads to increased atherosclerosis under atherosclerotic prone conditions.
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XO activity is increased by angiotensin II, TNF-α, LPS, IL-6, and hypoxia.
“XO is expressed in ECs (393), and its activity is increased by angiotensin II (551), TNF-α, LPS (117, 311), IL-6, and hypoxia (410, 748).”
From Sources of Vascular Nitric Oxide and Reactive Oxygen Species and Their Regulation (2019) · cites this paper as [551]
XO is indirectly activated by angiotensin II, increasing cellular ROS production.
“Secondary to the main role of mitochondria and NOX, but not to be ignored, XO and eNOS can also amplify the formation of ROS; for instance, XO is indirectly activated by angiotensin II, increasing cellular ROS production (551).”
From Sources of Vascular Nitric Oxide and Reactive Oxygen Species and Their Regulation (2019) · cites this paper as [551]
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- Authors
- Langbein, H., Brunssen, C., Hofmann, A., Cimalla, P., Brux, M., Bornstein, S. R., Deussen, A., Koch, E., & Morawietz, H.
- Affiliations
- University Hospital Carl Gustav Carus (DE)
- Technische Universität Dresden (DE)
- Corresponding author
- Morawietz, Henning
- Venue
- European Heart Journal
- Publisher
- Oxford University Press (OUP)
- Published
- 2015-11-17
- Volume
- 37
- Issue
- 22
- Pages
- 1753-1761
- ISSN
- 0195-668X (ISSN-L)
- 1522-9645
- PMC
- PMC4900759
- OpenAlex
- W2172883491
- Cited by
- 133
- References
- 53
- Citations by year
- 2026: 7 · 2025: 7 · 2024: 10 · 2023: 16 · 2022: 14 · 2021: 11 · 2020: 10 · 2019: 10 · 2018: 11 · 2017: 24 · 2016: 12 · 2015: 1
- FWCI
- 11.79
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- cc-by-nc
- Locations
- European Heart Journal (publishedVersion, cc-by-nc)
- PubMed Central (publishedVersion, cc-by-nc)
- PubMed (publishedVersion)
- Zurich Open Repository and Archive (University of Zurich) (acceptedVersion, cc-by-nc)
- HighWire Press Open Archive (submittedVersion)
- Zurich Open Repository and Archive (University of Zurich) (submittedVersion, cc-by-nc)
- Zurich Open Repository and Archive (University of Zurich)
- 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
- NOX4, endothelial dysfunction, atherosclerosis, LDL receptor deficiency, superoxide, hydrogen peroxide, nitric oxide synthase, flow-mediated dilation, galectin-3, atherosclerotic plaque, high-fat diet, saphenous artery, optical coherence tomography
- MeSH terms
- NADPH Oxidase 4, Animals, Hydrogen Peroxide, Mice, Inbred C57BL, Receptors, LDL, Mice, Knockout, NADPH Oxidases, Endothelial Cells, Atherosclerosis, Mice
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