title: The alpha1-adrenergic receptors in cardiac hypertrophy: signaling mechanisms and functional implications.
abstract: 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.
authors.affiliation: Dipartimento di Bioscienze, Biotecnologie e Biofarmaceutica, Università di Bari, Via Orabona 4, 70125 Bari, Italy. Electronic address: susanna.cotecchia@uniba.it.
authors.forename: Susanna
authors.initials: S
authors.lastname: Cotecchia
authors.affiliation: Department de Pharmacologie et de de Toxicologie, Université de Lausanne, Rue du Bugnon 27, 1005, Lausanne, Switzerland.
authors.forename: Cosmo Damiano
authors.initials: CD
authors.lastname: Del Vescovo
authors.affiliation: Dipartimento di Bioscienze, Biotecnologie e Biofarmaceutica, Università di Bari, Via Orabona 4, 70125 Bari, Italy.
authors.forename: Matilde
authors.initials: M
authors.lastname: Colella
authors.affiliation: Dipartimento di Bioscienze, Biotecnologie e Biofarmaceutica, Università di Bari, Via Orabona 4, 70125 Bari, Italy; Department de Pharmacologie et de de Toxicologie, Université de Lausanne, Rue du Bugnon 27, 1005, Lausanne, Switzerland.
authors.forename: Stefania
authors.initials: S
authors.lastname: Caso
authors.affiliation: Department de Pharmacologie et de de Toxicologie, Université de Lausanne, Rue du Bugnon 27, 1005, Lausanne, Switzerland.
authors.forename: Dario
authors.initials: D
authors.lastname: Diviani
mesh_terms: D000818:Animals; D006332:Cardiomegaly / Q000378:metabolism*; D006801:Humans; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D032383:Myocytes, Cardiac / Q000378:metabolism; D018340:Receptors, Adrenergic, alpha-1 / Q000502:physiology*; D015398:Signal Transduction; D020257:Ventricular Remodeling
chemical_list: D018340:Receptors, Adrenergic, alpha-1
keywords: A-Kinase-Anchoring Protein-Lbc; Alpha1-adrenergic receptors; Cardiac hypertrophy; G protein coupled receptors; MAP kinases; Rho signaling