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Cited by 135Aortic Disease and Treatment ApproachesNitric Oxide and Endothelin EffectsAortic aneurysm repair treatments

The DOI matches its Crossref record; 50 of the 50 references it cites were found in a registry or an index.

NOX1 Deficiency Protects From Aortic Dissection in Response to Angiotensin II

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Gavazzi, Gaetan, Deffert, Christine, Trocme, Candice, Schäppi, Michela, Herrmann, François R., Krause, Karl-Heinz·2007·Hypertension
DOI 10.1161/hypertensionaha.107.089706
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Abstract

Oxidative stress leads to vascular damage and participates in the pathomechanisms of aortic dissection and aneurysm formation. Here we study aortic dissection in mice deficient in the superoxide-generating reduced nicotinamide-adenine dinucleotide phosphate oxidase NOX1. Seven days of treatment with the hypertensive agent angiotensin II (3 mg/kg per day) led to aortic dissection in 23% of wild-type C57BL/6J mice but in only 4% of NOX1-deficient mice ( P =0.05). In contrast, treatment of wild-type C57BL/6J mice with the hypertensive agent norepinephrine (12 mg/kg per day), did not lead to aortic dissection or sudden death, suggesting that hypertension is not sufficient to cause aortic dissection. Interestingly, norepinephrine-dependent blood pressure elevations were conserved in NOX1-deficient mice, demonstrating that, different from angiotensin II, it acts through NOX1-independent hypertensive mechanisms. The resistance of NOX1-deficient mice to angiotensin II-induced aortic dissection suggests a role for NOX1-dependent alterations of the vascular wall. We, therefore, studied gene expression and protease/inhibitor equilibrium. cDNA array analysis demonstrated differential effects of angiotensin II on gene expression in wild-type and NOX1-deficient mice. Tissue inhibitor of metalloproteinase 1 was increased both on the mRNA and the protein level in aortas from NOX1-deficient mice. Thus, our results demonstrate that NOX1 is involved in the mechanisms of angiotensin II-dependent aortic dissection. As one underlying mechanism, we have identified NOX1-dependent suppression of tissue inhibitor of metalloproteinase 1 expression, which could lead to tissue damage through an altered protease/inhibitor balance.

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  1. 10.1161/hyp.38.6.1382 · DOI
  2. 10.1161/res.88.9.947 · DOI
  3. 10.1161/hyp.28.6.1064 · DOI
  4. 10.1161/circ.104.20.2391 · DOI

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Metadata

Authors
Gavazzi, G., Deffert, C., Trocme, C., Schäppi, M., Herrmann, F. R., & Krause, K.-H.
Affiliations
  • Centre National de la Recherche Scientifique (FR)
  • From the Department of Geriatrics (G.G.) and Groupe de Recherche et d’Etude du Processus Inflammatoire Techniques de I’Ingénierie Médicale et de la Complexité-Imag Unité Mixtede Recherche-Centre National de la Recherche Scientifique 5525 (G.G., C.T.), University Hospital of Grenoble, Grenoble, France; and the Departments of Pathology, Immunology, and Clinical Pathology (C.D., M.S., K-H.K.), Pediatrics (C.D.), and Rehabilitation and Geriatrics (F.R.H.), Geneva Medical Faculty, Geneva, Switzerland.
ORCID
Venue
Hypertension
Publisher
Ovid Technologies (Wolters Kluwer Health)
Published
2007-07
Volume
50
Issue
1
Pages
189-196
ISSN
  • 0194-911X (ISSN-L)
  • 1524-4563
DOI
10.1161/hypertensionaha.107.089706
OpenAlex
W2140545013
Cited by
135
References
50
Citations by year
2026: 1 · 2025: 3 · 2024: 9 · 2023: 2 · 2022: 5 · 2021: 5 · 2020: 6 · 2019: 5 · 2018: 9 · 2017: 3 · 2016: 10 · 2015: 8 · 2014: 7 · 2013: 11 · 2012: 8
FWCI
8.93
Type
journal article
Language
en
Open access
Licence
cc-by
Locations
  • Hypertension (publishedVersion)
  • PubMed (publishedVersion)
  • HAL (submittedVersion)
  • Archive ouverte UNIGE (University of Geneva) (submittedVersion, cc-by)
Funders
Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung
Topics
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Aortic Disease and Treatment Approaches
  • Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
  • Health Sciences › Medicine › Surgery › Aortic aneurysm repair treatments
Keywords
NOX1, aortic dissection, angiotensin II, oxidative stress, NADPH oxidase, norepinephrine, TIMP-1, protease-inhibitor balance, vascular wall damage, gene expression, sudden death
MeSH terms
NADPH Oxidase 1, Aortic Dissection, Angiotensin II, Animals, Aorta, Thoracic, Aortic Aneurysm, Blood Pressure, Disease Susceptibility, Gene Expression Regulation, Hypertension, Male, Mice, Inbred C57BL, Norepinephrine, RNA, Messenger, Vasoconstrictor Agents, Mice, Knockout, NADPH Oxidases, Tissue Inhibitor of Metalloproteinase-1, Matrix Metalloproteinase 2, Matrix Metalloproteinase 9, Mice

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