title: Alteration of the beta-adrenergic signaling pathway in human heart failure.
abstract: Heart failure is characterized by elevated circulating catecholamine levels and extensive abnormalities in β-adrenergic receptor signaling. Under physiological conditions, sympathetic modulation via catecholamines induces positive inotropic, chronotropic and lusitropic responses. Well established in heart failure patients is a pronounced activation of the sympathetic system, accompanied by downregulation and desensitization of β-adrenergic receptors, leading to a markedly diminished β-adrenergic contractile response. In this review, we will discuss the normal β-adrenergic receptor signaling pathway in the heart and focus on the pathphysiological alterations of β-adrenergic receptor signaling and contractile proteins in heart failure.
authors.affiliation: Department of Cardiovascular Physiology, Institute of Physiology, Ruhr University Bochum, MA 3/56, D-44780 Bochum, Germany. Nazha.Hamdani@rub.de
authors.forename: Nazha
authors.initials: N
authors.lastname: Hamdani
authors.forename: Wolfgang A
authors.initials: WA
authors.lastname: Linke
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000008:administration & dosage / Q000627:therapeutic use; D015536:Down-Regulation; D006333:Heart Failure / Q000188:drug therapy / Q000378:metabolism* / Q000503:physiopathology; D006801:Humans; D008840:Microfilament Proteins / Q000378:metabolism; D009200:Myocardial Contraction / Q000187:drug effects; D009210:Myofibrils / Q000378:metabolism; D010766:Phosphorylation; D011943:Receptors, Adrenergic, beta / Q000235:genetics / Q000378:metabolism*; D015398:Signal Transduction
chemical_list: D000319:Adrenergic beta-Antagonists; D008840:Microfilament Proteins; D011943:Receptors, Adrenergic, beta