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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
Online ISSN 1827-1618
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.