Focal adhesion kinase governs cardiac concentric hypertrophic growth by activating the AKT and mTOR pathways

► Hypertrophy can be adaptive or pathological. ► Cardiac myocyte-FAK overexpression in mice induced compensated cardiac hypertrophy. ► Upregulation of FAK was accompanied by activation of PI3K, AKT, mTOR, S6K and rpS6. ► Inhibition of the mTOR complex by rapamycin extinguished the cardiac hypertrophy. ► FAK activation may be important for the adaptive responses to increases in cardiac afterload.