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.
Keywords: Heart failure, β adrenergic receptors, myofilament proteins, cardiomyocytes
Current Pharmaceutical Biotechnology
Title:Alteration of the Beta-Adrenergic Signaling Pathway in Human Heart Failure
Volume: 13 Issue: 13
Author(s): Nazha Hamdani and Wolfgang A. Linke
Affiliation:
Keywords: Heart failure, β adrenergic receptors, myofilament proteins, cardiomyocytes
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.
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Cite this article as:
Hamdani Nazha and A. Linke Wolfgang, Alteration of the Beta-Adrenergic Signaling Pathway in Human Heart Failure, Current Pharmaceutical Biotechnology 2012; 13 (13) . https://dx.doi.org/10.2174/1389201011208062522
DOI https://dx.doi.org/10.2174/1389201011208062522 |
Print ISSN 1389-2010 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4316 |
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