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

Copyright © 2001 EDIZIONI MINERVA MEDICA

language: English

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.


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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.

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