Decreased blood pressure in NOX1‐deficient mice

Gavazzi, Gaetan; Banfi, Botond; Deffert, Christine; Fiette, Laurence; Schappi, Michela; Herrmann, Francois; Krause, Karl-Heinz

doi:10.1016/j.febslet.2005.12.049

Cited by 321Nitric Oxide and Endothelin EffectsRenin-Angiotensin System StudiesEicosanoids and Hypertension Pharmacology

Decreased blood pressure in NOX1‐deficient mice

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Gavazzi, Gaetan, Banfi, Botond, Deffert, Christine, Fiette, Laurence, Schappi, Michela, Herrmann, Francois, Krause, Karl-Heinz·2006·FEBS Letters

DOI 10.1016/j.febslet.2005.12.049

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Abstract

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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Nox1-KO mice used were derived from at least 10 backcrosses with WT C57BL/6J mice.
“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
The role of NOX1 in cardiovascular disease seems secondary to NOX2, but still significant, as shown in several models.
“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]
NOX1 deletion limits the blood pressure increase elicited by angiotensin II.
“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]
Nox1, 3, 4, 5, and Duox1 and 2 usually produce smaller amounts of ROS for regulation of signaling pathways or during anabolic processes.
“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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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
ORCID: Gavazzi, Gaetan
Deffert, Christine
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
DOI: 10.1016/j.febslet.2005.12.049
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: green
archive-ouverte.unige.ch
Licence: cc-by
onlinelibrary.wiley.com/termsAndConditions#vor (vor)
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 › 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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Decreased blood pressure in NOX1‐deficient mice

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