The DOI matches its Crossref record; 27 of the 28 references it cites were found in a registry or an index.
Endothelial-specific Nox2 overexpression increases vascular superoxide and macrophage recruitment in ApoE−/− mice
Open accessAbstract
AIMS: Vascular disease states are associated with endothelial dysfunction and increased production of reactive oxygen species derived from NADPH oxidases. However, it remains unclear whether a primary increase in superoxide production specifically in the endothelium alters the initiation or progression of atherosclerosis. METHODS AND RESULTS: Mice overexpressing Nox2 specifically in the endothelium (Nox2-Tg) were crossed with ApoE(-/-) mice to produce Nox2-Tg ApoE(-/-) mice and ApoE(-/-) littermates. Endothelial overexpression of Nox2 in ApoE(-/-) mice did not alter blood pressure, but significantly increased vascular superoxide production compared with ApoE(-/-) littermates, measured using both lucigenin chemiluminescence and 2-hydroxyethidium production (ApoE(-/-), 19.9 ± 6.3 vs. Nox2-Tg ApoE(-/-), 47.0 ± 7.0 nmol 2-hydroxyethidium/aorta, P< 0.05). Increased endothelial superoxide production increased endothelial levels of vascular cell adhesion protein 1 and enhanced macrophage recruitment in early lesions in the aortic roots of 9-week-old mice, indicating increased atherosclerotic plaque initiation. However, endothelial-specific Nox2 overexpression did not alter native or angiotensin II-driven atherosclerosis in either the aortic root or the descending aorta. CONCLUSION: Endothelial-targeted Nox2 overexpression in ApoE(-/-) mice is sufficient to increase vascular superoxide production and increase macrophage recruitment possible via activation of endothelial cells. However, this initial increase in macrophage recruitment did not alter the progression of atherosclerosis. These results indicate that Nox-mediated reactive oxygen species signalling has important cell-specific and distinct temporal roles in the initiation and progression of atherosclerosis.
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“However, in other cases, an increased expression of endothelial NOX2 has not been linked to pathological conditions even though an increased production of superoxide and macrophage recruitment was observed (243, 443).”
From Sources of Vascular Nitric Oxide and Reactive Oxygen Species and Their Regulation (2019) · cites this paper as [243]
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“The current paradigm indicates that macrophage NOX2 is more detrimental in the development of cardiovascular disease (395, 876), with endothelial NOX2 probably involved in the initiation, but not so much in the development of the disease, and a subsequent progress of the atherosclerotic lesion dependent on immune cells (243, 573, 976).”
From Sources of Vascular Nitric Oxide and Reactive Oxygen Species and Their Regulation (2019) · cites this paper as [243]
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“The current paradigm indicates that macrophage NOX2 is more detrimental in the development of cardiovascular disease (395, 876), with endothelial NOX2 probably involved in the initiation, but not so much in the development of the disease, and a subsequent progress of the atherosclerotic lesion dependent on immune cells (243, 573, 976).”
From Sources of Vascular Nitric Oxide and Reactive Oxygen Species and Their Regulation (2019) · cites this paper as [243]
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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
ApoE-deficient mice develop lesions of all phases of atherosclerosis throughout the arterial tree.
Nakashima, Y., Plump, A. S., Raines, E. W., Breslow, J. L., & Ross, R. (1994) · Arteriosclerosis and Thrombosis: A Journal of Vascular Biology · doi:10.1161/01.atv.14.1.133 · Cited by 1,693
Mechanisms of Increased Vascular Superoxide Production in Human Diabetes Mellitus
Guzik, T. J., Mussa, S., Gastaldi, D., Sadowski, J., Ratnatunga, C., Pillai, R. G., & Channon, K. M. (2002) · Circulation · doi:10.1161/01.cir.0000012748.58444.08 · Cited by 979
Self-citationSuperoxide Production and Expression of Nox Family Proteins in Human Atherosclerosis
Sorescu, D., Weiss, D., Lassègue, B., Clempus, R. E., Szöcs, K., Sorescu, G. P., Valppu, L., Quinn, M. T., Lambeth, J. D., Vega, J. D., et al. (2002) · Circulation · doi:10.1161/01.cir.0000012917.74432.66 · Cited by 847
Lassègue, B., Sorescu, D., Szöcs, K., Yin, Q., Akers, M., Zhang, Y., Grant, S. L., Lambeth, J. D., & Griendling, K. K. (2001) · Circulation Research · doi:10.1161/hh0901.090299 · Cited by 839
NADPH Oxidases in Cardiovascular Health and Disease
Cave, A. C., Brewer, A. C., Narayanapanicker, A., Ray, R., Grieve, D. J., Walker, S., & Shah, A. M. (2006) · Antioxidants & Redox Signaling · doi:10.1089/ars.2006.8.691 · Cited by 630
Görlach, A., Brandes, R. P., Nguyen, K., Amidi, M., Dehghani, F., & Busse, R. (2000) · Circulation Research · doi:10.1161/01.res.87.1.26 · Cited by 598
NADPH Oxidases: Functions and Pathologies in the Vasculature
Lassègue, B., & Griendling, K. K. (2010) · Arteriosclerosis, Thrombosis, and Vascular Biology · doi:10.1161/atvbaha.108.181610 · Cited by 592
Vascular Superoxide Production by NAD(P)H Oxidase
Guzik, T. J., West, N. E. J., Black, E., McDonald, D., Ratnatunga, C., Pillai, R. G., & Channon, K. M. (2000) · Circulation Research · doi:10.1161/01.res.86.9.e85 · Cited by 584
Self-citationPueyo, M. E., Gonzalez, W., Nicoletti, A., Savoie, F., Arnal, J., & Michel, J. (2000) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/01.atv.20.3.645 · Cited by 523
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Metabolic study of Alzheimer’s disease using mutant C. elegans
Ahmad, W. (2017) · The University of Queensland · doi:10.14264/uql.2017.500
Thiriet, M., Delfour, M. C., & Garon, A. (2014) · Springer eBooks · doi:10.1007/978-3-642-37393-0_32-1 · Cited by 1
Vascular Reactive Oxygen Species Biology – Insights from Transgenic and Knockout Mouse Models
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Fronczek, M., Banach, M., Goławski, M., & Osadnik, T. (2025) · Elsevier eBooks · doi:10.1016/b978-0-443-27333-9.00013-0
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RetractedChemokines and redox homeostasis in aging: A dynamic relationship
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Metadata
- Authors
- Douglas, G., Bendall, J. K., Crabtree, M. J., Tatham, A. L., Carter, E. E., Hale, A. B., & Channon, K. M.
- Affiliations
- John Radcliffe Hospital (GB)
- University of Oxford (GB)
- Corresponding author
- Douglas, Gillian
- Venue
- Cardiovascular Research
- Publisher
- Oxford University Press (OUP)
- Published
- 2012-01-27
- Volume
- 94
- Issue
- 1
- Pages
- 20-29
- ISSN
- 0008-6363 (ISSN-L)
- 1755-3245
- PMC
- PMC3307381
- OpenAlex
- W1988097865
- Cited by
- 111
- References
- 28
- Citations by year
- 2026: 5 · 2025: 5 · 2024: 8 · 2023: 7 · 2022: 12 · 2021: 5 · 2020: 1 · 2019: 6 · 2018: 8 · 2017: 13 · 2016: 10 · 2015: 6 · 2014: 10 · 2013: 10 · 2012: 5
- FWCI
- 6.65
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- other-oa
- Locations
- Cardiovascular Research (publishedVersion, other-oa)
- PubMed Central (publishedVersion, cc-by-nc)
- PubMed (publishedVersion)
- Funders
- Wellcome Trust (090532)
- British Heart Foundation (PG/05/141/20098, RG/07/003/23133, RG/12/5/29576)
- Topics
- Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Life Sciences › Immunology and Microbiology › Immunology › Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Keywords
- NOX2, NADPH oxidase, atherosclerosis initiation, macrophage recruitment, ApoE-deficient mice, VCAM-1, reactive oxygen species, endothelial dysfunction, angiotensin II, aortic root lesions
- MeSH terms
- NADPH Oxidase 2, Angiotensin II, Animals, Aortic Diseases, Apolipoproteins E, Blood Pressure, Chemotaxis, Disease Models, Animal, Humans, Macrophages, Membrane Glycoproteins, Mice, Transgenic, Superoxides, Time Factors, Signal Transduction, Up-Regulation, Mice, Knockout, Disease Progression, Vascular Cell Adhesion Molecule-1, NADPH Oxidases, Endothelial Cells, Atherosclerosis, Mice
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