Angiotensin II as an Inducer of Atherosclerosis: Evidence from Mouse Studies

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Ressource 1Télécharger: BIB_E6568726F216.P001.pdf (1505.63 [Ko])
Etat: Public
Version: Final published version
Licence: Non spécifiée
ID Serval
serval:BIB_E6568726F216
Type
Article: article d'un périodique ou d'un magazine.
Sous-type
Synthèse (review): revue aussi complète que possible des connaissances sur un sujet, rédigée à partir de l'analyse exhaustive des travaux publiés.
Collection
Publications
Institution
Titre
Angiotensin II as an Inducer of Atherosclerosis: Evidence from Mouse Studies
Périodique
Journal of Clinical and Experimental Cardiology
Auteur⸱e⸱s
Pellegrin M., Mazzolai L.
ISSN
2155-9880
ISSN-L
2155-9880
Statut éditorial
Publié
Date de publication
2013
Volume
1
Numéro
S1
Pages
007
Langue
anglais
Notes
pdf type: review article
Copyright: © 2013 Pellegrin M, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Résumé
Mechanisms responsible for atherosclerotic plaque development, destabilization, and rupture are still largely unknown. Angiotensin II, the main bioactive peptide of renin angiotensin system, has been shown to be critically involved in the pathogenesis of atherosclerosis and vulnerable plaque. Experimental studies in hypercholesterolemic mouse models with high circulating Angiotensin II levels, provide direct evidence that Angiotensin II induces plaque vulnerability partly by 1/ downregulating vascular expression of anti-atherosclerotic genes and/or upregulating expression of pro-atherosclerotic genes, and 2/ skewing the systemic lymphocyte Th1/Th2 balance towards a proinflammatory Th1 response in early disease phase. Further understanding the pro-atherosclerotic mechanisms of Angiotensin II and associated signaling pathways will help to design better therapeutic strategies for reducing the burden of atherosclerotic cardiovascular disease.
Open Access
Oui
Création de la notice
12/02/2014 14:47
Dernière modification de la notice
10/05/2023 5:53
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