The major findings of this study were: (1) rTM suppressed stress-induced autophagy overactivation in ECs; (2) autophagy modulated ECs cell behavior; (3) autophagy was activated in aortic ECs in human atherosclerosis and apoE deficient mice; (4) rTM treatment suppressed aortic ECs autophagy and decreased atherosclerosis in apoE deficient mice and (5) rTM effect on autophagy was achieved through mTOR activation via the FGFR1/FRS2α-mediated PI3K/AKT pathway. Here, FGFR1 is linked to atherosclerosis.