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Home > Journals > Minerva Cardioangiologica > Past Issues > Minerva Cardioangiologica 2001 December;49(6) > Minerva Cardioangiologica 2001 December;49(6):389-94



A Journal on Heart and Vascular Diseases

Official Journal of the Italian Society of Angiology and Vascular Pathology
Indexed/Abstracted in: EMBASE, PubMed/MEDLINE, Science Citation Index Expanded (SciSearch), Scopus
Impact Factor 0,752

Frequency: Bi-Monthly

ISSN 0026-4725

Online ISSN 1827-1618


Minerva Cardioangiologica 2001 December;49(6):389-94


Gene-mediated inhibition of the beta-adrenergic receptor kinase: a new therapeutic strategy for heart failure

Tevaearai H. T., Eckhart A. D., Koch W. J.

Molecular changes that take place during the evolution of heart failure (HF), especially the well characterized b-adrenergic receptor (bAR) signaling abnormalities, represent attractive targets for myocardial gene therapy. The b-adrenergic receptor kinase (bARK1 or GRK2) is a cytosolic enzyme that phosphorylates only agonist-occupied bARs as well as other G protein-coupled receptors (GPCRs), leading to desensitization and functional uncoupling. bARK1 levels and activity are elevated in the failing heart and therefore, it has recently been evaluated as a potential target for novel HF treatment. This review summarizes recent results obtained in transgenic mouse models as well as in animals where a bARK1 inhibitor peptide (bARKct) was delivered via the coronary arteries by exogenous gene transfer. These results strongly suggest that bARK1 inhibition may represent a significant improvement in HF therapy.

language: English

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