Open AccessSmall Molecule Disruption of Gβγ Signaling Inhibits the Progression of Heart Failure
Author(s) -
Liam M. Casey,
Andrew Pistner,
Stephen L. Belmonte,
Dmitriy Migdalovich,
Olga Stolpnik,
Frances E. Nwakanma,
Gabriel Vorobiof,
Olga Dunaevsky,
Alessandra Matavel,
Coeli M. Lopes,
Alan V. Smrcka,
Burns C. Blaxall
Publication year - 2010
Publication title -
circulation research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.899
H-Index - 336
eISSN - 1524-4571
pISSN - 0009-7330
DOI - 10.1161/circresaha.110.217075
Subject(s) - beta adrenergic receptor kinase , heart failure , agonist , medicine , signal transduction , g protein coupled receptor kinase , receptor , endocrinology , pharmacology , contractility , downregulation and upregulation , chemistry , biology , g protein , microbiology and biotechnology , g protein coupled receptor , biochemistry , gene
Excess signaling through cardiac Gbetagamma subunits is an important component of heart failure (HF) pathophysiology. They recruit elevated levels of cytosolic G protein-coupled receptor kinase (GRK)2 to agonist-stimulated beta-adrenergic receptors (beta-ARs) in HF, leading to chronic beta-AR desensitization and downregulation; these events are all hallmarks of HF. Previous data suggested that inhibiting Gbetagamma signaling and its interaction with GRK2 could be of therapeutic value in HF.
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