Table of Contents
Journal of Signal Transduction
Volume 2011, Article ID 521742, 8 pages
Review Article

Integrins Are the Necessary Links to Hypertrophic Growth in Cardiomyocytes

1Cardiology Division, Department of Medicine, Gazes Cardiac Research Institute, Medical University of South Carolina, Charleston, SC 29425-2221, USA
2Advanced BioScience Laboratories, Inc., 5510 Nicholson Lane, Kensington, MD 20895, USA

Received 21 October 2010; Accepted 15 December 2010

Academic Editor: Wan-Wan Lin

Copyright © 2011 Rebecca K. Harston and Dhandapani Kuppuswamy. 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.


To compensate for hemodynamic overload of the heart, an event which stretches the myocardium, growth and survival signaling are activated in cardiac muscle cells (cardiomyocytes). Integrins serve as the signaling receptors of cardiomyocytes responsible for mechanotransduction toward intracellular signaling. The main integrin heterodimers on the cardiomyocyte surface are α5β1 and , and elimination of either β1 or β3 integrins impedes pressure-induced hypertrophic signaling and leads to increased mortality. The growth signaling pathways downstream of β1 and β3 integrins are well characterized. However, new integrin pathways responsible for inhibiting apoptosis induced by hemodynamic overload are emerging. β1 and β3 integrins activate differential survival signaling, yet both integrins initiate survival signaling downstream of ubiquitination and the kinase pathway including phosphoinositol-3-kinase (PI3K)/Akt. Further characterization of these integrin-signaling mechanisms may lead to drug targets to prevent decompensation to heart failure.