Integrins are the necessary links to hypertrophic growth in cardiomyocytes.

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 α(5)ß(1) and α(v)ß(3), and elimination of either ß(1) or ß(3) integrins impedes pressure-induced hypertrophic signaling and leads to increased mortality. The growth signaling pathways downstream of ß(1) and ß(3) integrins are well characterized. However, new integrin pathways responsible for inhibiting apoptosis induced by hemodynamic overload are emerging. ß(1) and ß(3) 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.