The DOI matches its Crossref record; 43 of the 43 references it cites were found in a registry or an index.
Decreased blood pressure in NOX1‐deficient mice
Open accessAbstract
To understand the role of the superoxide‐generating NADPH oxidase NOX1 in the vascular system, we have generated NOX1‐deficient mice. NOX1‐deficient mice had a moderately decreased basal blood pressure. In response to angiotensin II they showed an almost complete loss of the sustained blood pressure response, while the initial increase was conserved. NOX1‐deficient mice showed a marked reduction in aortic media hypertrophy. Angiotensin II‐induced smooth muscle cell proliferation was conserved, but there was a marked decrease in extracellular matrix accumulation. Our results establish a role for NOX1 in blood pressure regulation and vascular angiotensin II response.
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In the citing paper
“Nox1-KO mice (Gavazzi et al., 2006) used in our experiments were derived from at least 10 backcrosses with WT C57BL/6J mice.”
From Neurotoxic Activation of Microglia Is Promoted by a Nox1-Dependent NADPH Oxidase (2008) · cites this paper as Gavazzi et al., 2006
In the citing paper
“Altogether, the role of NOX1 in cardiovascular disease seems secondary to NOX2, but still significant, as shown in several models (345, 380, 630, 854).”
From Sources of Vascular Nitric Oxide and Reactive Oxygen Species and Their Regulation (2019) · cites this paper as [345]
In the citing paper
“NOX1 deletion limits the blood pressure increase elicited by angiotensin II, although it is unclear if basal blood pressure levels are reduced (345, 346, 630).”
From Sources of Vascular Nitric Oxide and Reactive Oxygen Species and Their Regulation (2019) · cites this paper as [345]
In the citing paper
“Nox1, 3, 4, 5, and Duox1 and 2 usually produce smaller amounts of ROS for regulation of signaling pathways or during anabolic processes such as endothelial vasoregulation or synthesis of thyroid hormones [94,95,96,97,98].”
From Functions of ROS in Macrophages and Antimicrobial Immunity (2021) · cites this paper as [97]
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Metadata
- Authors
- Gavazzi, G., Banfi, B., Deffert, C., Fiette, L., Schappi, M., Herrmann, F., & Krause, K.-H.
- Affiliations
- University of Geneva (CH)
- Corresponding author
- Krause, Karl-Heinz
- Venue
- FEBS Letters
- Publisher
- Wiley
- Published
- 2005-12-22
- Volume
- 580
- Issue
- 2
- Pages
- 497-504
- ISSN
- 0014-5793 (ISSN-L)
- 1873-3468
- OpenAlex
- W2123617367
- Cited by
- 321
- References
- 42
- Citations by year
- 2026: 2 · 2025: 6 · 2024: 10 · 2023: 8 · 2022: 4 · 2021: 18 · 2020: 19 · 2019: 20 · 2018: 12 · 2017: 10 · 2016: 21 · 2015: 18 · 2014: 29 · 2013: 19 · 2012: 27
- FWCI
- 7.42
- Type
- journal article
- Language
- en
- Open access
- Locations
- FEBS Letters (publishedVersion)
- PubMed (publishedVersion)
- HAL (submittedVersion)
- Archive ouverte UNIGE (University of Geneva) (submittedVersion, cc-by)
- Archive ouverte UNIGE (University of Geneva) (submittedVersion)
- Topics
- Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Renin-Angiotensin System Studies
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Eicosanoids and Hypertension Pharmacology
- Keywords
- NOX1, NADPH oxidase, blood pressure regulation, angiotensin II, vascular smooth muscle cells, extracellular matrix accumulation, superoxide, hypertension
- MeSH terms
- NADPH Oxidase 1, Angiotensin II, Animals, Blood Pressure, Extracellular Matrix, Female, Hypotension, Male, Mice, Inbred C57BL, Muscle, Smooth, Vascular, NADH, NADPH Oxidoreductases, Signal Transduction, Tunica Media, Mice, Knockout, Cell Proliferation, Mice
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