MTOR and hypertensive disorder: Conclusively, the present study shows that SU induces hypertension and left ventricular dysfunction in mice and cell viability loss in H9c2 cardiomyocytes via inhibition of AMPK/mTOR/autophagy pathway; trimetazidine is able to reverse sunitinib-induced cardiotoxicity in mice as well as viability loss in H9c2 cardiomyocytes via involvement of AMPK/mTOR/autophagy pathway activation.