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• W2468767034 abstract "Significance Commonly prescribed drugs for congestive heart failure (CHF) include β-adrenergic receptor antagonists or β-blockers. These drugs operate by inhibiting deleterious apoptotic signaling and normalizing inotropic signaling from these receptors. As the β-adrenergic receptor (β 1 AR) (dominant subtype in the heart) is systematically down-regulated during CHF while G i (a G protein that antagonizes contractile signaling) is up-regulated, the ability to selectively control β 2 AR signaling becomes an attractive therapeutic approach. It is proposed that biasing receptor interaction with β-arrestins (promoting antiapoptotic signaling and possibly contraction) over G proteins may be therapeutically advantageous for the treatment of CHF. Here, we report a β-arrestin–biased pepducin of the β 2 AR that is able to induce cardiomyocyte contractility and antiapoptotic signaling to provide a pharmacological template for next-generation cardiovascular pharmaceuticals." @default.
• W2468767034 created "2016-07-22" @default.
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• W2468767034 date "2016-06-27" @default.
• W2468767034 modified "2023-10-11" @default.
• W2468767034 title "β-arrestin–biased signaling through the β ₂ -adrenergic receptor promotes cardiomyocyte contraction" @default.
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• W2468767034 doi "https://doi.org/10.1073/pnas.1606267113" @default.
• W2468767034 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4948363" @default.
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