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JCI table of contents: Sept. 4, 2007
Date:9/4/2007

beta1-adrenergic receptor in the heart that protects the muscle cells of the heart from dying. The potential clinical impact of these observations is discussed in the accompanying commentary by Stefan Englehardt from the University of Würzburg, Germany.

In the study, stimulation of the beta1-adrenergic receptor, in vitro in human and mouse cells and in vivo in mice, was shown to activate a beta-arrestin signaling pathway that required the G protein–coupled receptor kinases 5 and 6 and resulted in transactivation of EGFR. Signaling downstream of EGFR activation protected the heart muscle cells from the toxic effects of chronic signals from the beta1-adrenergic receptor transmitted through Gs-dependent adenylyl cyclase activation. The latter signals are associated with heart failure and so the authors suggest that drugs that block Gs-dependent adenylyl cyclase activation but activate beta-arrestin signaling might provide a new type of therapeutic for the prevention of heart failure.

TITLE: Beta-Arrestin–mediated beta1-adrenergic receptor transactivation of the EGFR confers cardioprotection

AUTHOR CONTACT:

Howard A. Rockman
Duke University Medical Center, Durham, North Carolina, USA.
Phone: (919) 668-2520; Fax: (919) 668-2524; E-mail: h.rockman@duke.edu.

View the PDF of this article at: https://www.the-jci.org/article.php?id=31901

ACCOMPANYING COMMENTARY

TITLE: Alternative signaling: cardiomyocyte beta1-adrenergic receptors signal through EGFRs

AUTHOR CONTACT:

Stefan Engelhardt
University of Würzburg, Würzburg, Germany..
Phone: 49-931-201-48710; Fax: 49-931-201-48123; E-mail: stefan.engelhardt@virchow.uni-wuerzburg.de.

View the PDF of this article at:

Contact: Karen Honey
press_releases@the-jci.org
215-573-1850
Journal of Clinical Investigation
Source:Eurekalert

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