It was revealed to reduce excessive extracellular matrix deposition and attenuate myocardial injury and myocardial fibrosis, possibly through stimulating the AMPK/mTOR pathway, improving LC3 and Beclin-1expression, and activating autophagy, which in turn restrains the TGF-β/matrix metalloproteinase pathway (84). Here, MTOR is linked to Myocardial fibrosis.