In keeping with this, pharmacological inhibition of mTOR signaling using Rapamycin was documented to regress both compensatory and decompensatory cardiac hypertrophy in mice subjected to aortic constriction [54], whereas mTORC2 disruption was accompanied by suppression of compensatory cardiac growth, marked apoptosis and decreased contractile performance in response to pressure overload [55,56], underlying the overall importance of the two mTOR signaling branches in the adaptation of mechanical injury. Here, MTOR is linked to cardiac hypertrophy.