The alpha1-adrenergic receptors in cardiac hypertrophy: Signaling mechanisms and functional implications.

Détails

ID Serval
serval:BIB_63C854825011
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
Titre
The alpha1-adrenergic receptors in cardiac hypertrophy: Signaling mechanisms and functional implications.
Périodique
Cellular Signalling
Auteur(s)
Cotecchia S., Del Vescovo C.D., Colella M., Caso S., Diviani D.
ISSN
1873-3913 (Electronic)
ISSN-L
0898-6568
Statut éditorial
Publié
Date de publication
2015
Peer-reviewed
Oui
Volume
27
Numéro
10
Pages
1984-1993
Langue
anglais
Notes
Document Type: Review
Résumé
Cardiac hypertrophy is a complex remodeling process of the heart induced by physiological or pathological stimuli resulting in increased cardiomyocyte size and myocardial mass. Whereas cardiac hypertrophy can be an adaptive mechanism to stressful conditions of the heart, prolonged hypertrophy can lead to heart failure which represents the primary cause of human morbidity and mortality. Among G protein-coupled receptors, the α1-adrenergic receptors (α1-ARs) play an important role in the development of cardiac hypertrophy as demonstrated by numerous studies in the past decades, both in primary cardiomyocyte cultures and genetically modified mice. The results of these studies have provided evidence of a large variety of α1-AR-induced signaling events contributing to the defining molecular and cellular features of cardiac hypertrophy. Recently, novel signaling mechanisms have been identified and new hypotheses have emerged concerning the functional role of the α1-adrenergic receptors in the heart. This review will summarize the main signaling pathways activated by the α1-AR in the heart and their functional implications in cardiac hypertrophy.
Pubmed
Web of science
Création de la notice
05/10/2015 12:20
Dernière modification de la notice
20/08/2019 14:20
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