Β-arrestin: a signaling molecule and potential therapeutic target for heart failure.

Published

Journal Article (Review)

Currently, some of the most effective treatments for heart failure target GPCRs such as the beta-adrenergic receptors (β1AR and β2AR) and angiotensin II type IA receptors (AT1aR). Ligands for these receptors not only function by blocking the deleterious G-protein mediated pathway leading to heart failure, but also signal via G-protein independent pathways that involve receptor phosphorylation by G-protein receptor kinases (GRKs) leading to recruitment of the multifunctional protein, β-arrestin. Originally thought to play a role in GPCR desensitization and internalization, β-arrestin has recently been shown to mediate signaling independent of classical second messengers in a way that is often protective to the heart. The multi-functionality of β-arrestin makes it an intriguing molecule in the development of the next generation of drugs for cardiac diseases with the potential to simultaneously inhibit deleterious G-protein dependent pathways while activating beneficial β-arrestin mediated signaling. In this review, we explore various facets of β-arrestin signaling and offer a perspective on its potential role as a key signaling molecule in the treatment of heart failure. This article is part of a special issue entitled "Key Signaling Molecules in Hypertrophy and Heart Failure."

Full Text

Duke Authors

Cited Authors

  • Noor, N; Patel, CB; Rockman, HA

Published Date

  • October 2011

Published In

Volume / Issue

  • 51 / 4

Start / End Page

  • 534 - 541

PubMed ID

  • 21074538

Pubmed Central ID

  • 21074538

Electronic International Standard Serial Number (EISSN)

  • 1095-8584

Digital Object Identifier (DOI)

  • 10.1016/j.yjmcc.2010.11.005

Language

  • eng

Conference Location

  • England