title: Defects in cardiomyocyte function: role of beta-adrenergic receptor dysfunction.
abstract: Heart failure is a common clinical syndrome characterized by increased levels of circulating catecholamines and extensive abnormalities in the beta-adrenergic receptor (betaAR) system. Interestingly, whether dampening of betaAR signals is beneficial or detrimental for the failing cardiomyocyte is still controversial. In this review we will discuss a number of studies addressing the role of betaAR dysfunction in the development and progression of cardiomyocyte failure, and novel possible strategies to ameliorate cardiomyocyte contractility in heart failure through the normalization of betaAR signaling.
authors.affiliation: Department of Medicine, Cell Biology and Molecular Genetics, Duke University Medical Center, Durham, NC, USA.
authors.forename: C
authors.initials: C
authors.lastname: Perrino
authors.forename: G
authors.initials: G
authors.lastname: Esposito
authors.forename: H A
authors.initials: HA
authors.lastname: Rockman
mesh_terms: D000818:Animals; D054769:G-Protein-Coupled Receptor Kinase 2; D006333:Heart Failure / Q000503:physiopathology*; D006801:Humans; D009200:Myocardial Contraction; D032383:Myocytes, Cardiac / Q000502:physiology*; D000081082:Phosphoinositide-3 Kinase Inhibitors; D011943:Receptors, Adrenergic, beta / Q000502:physiology*; D015398:Signal Transduction; D051552:beta-Adrenergic Receptor Kinases / Q000037:antagonists & inhibitors
chemical_list: D000081082:Phosphoinositide-3 Kinase Inhibitors; D011943:Receptors, Adrenergic, beta; C496567:GRK2 protein, human; D051552:beta-Adrenergic Receptor Kinases; D054769:G-Protein-Coupled Receptor Kinase 2