Table of Contents
Journal of Signal Transduction
Volume 2011, Article ID 179057, 9 pages
Review Article

-Adrenergic Receptor-Stimulated Cardiac Myocyte Apoptosis: Role of 1 Integrins

Department of Physiology, James H Quillen Veterans Affairs Medical Center, James H Quillen College of Medicine, East Tennessee State University, P.O. Box 70576, Johnson City, TN 37614, USA

Received 2 December 2010; Revised 28 January 2011; Accepted 16 March 2011

Academic Editor: Terry Hebert

Copyright © 2011 Parthiv Amin et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Increased sympathetic nerve activity to the myocardium is a central feature in patients with heart failure. Accumulation of catecholamines plays an important role in the pathogenesis of heart disease. Acting via -adrenergic receptors ( -AR), catecholamines (norepinephrine and isoproterenol) increase cardiac myocyte apoptosis in vitro and in vivo. Specifically, 1-AR and 2-AR coupled to G s exert a proapoptotic action, while 2-AR coupled to Gi exerts an antiapoptotic action. 1 integrin signaling protects cardiac myocytes against -AR-stimulated apoptosis in vitro and in vivo. Interaction of matrix metalloproteinase-2 (MMP-2) with 1 integrins interferes with the survival signals initiated by 1 integrins. This paper will discuss background information on -AR and integrin signaling and summarize the role of 1 integrins in -AR-stimulated cardiac myocyte apoptosis.