These findings indicated that AE alleviated fibrosis by inhibiting PI3K/Akt/mTOR pathway <i>in vivo</i> and <i>in vitro</i>, which may provide a potential therapeutic option for CKD.
Here we examined the hypothesis that impairment of protective PI3K-PDK1-Akt and/or mTORC-Akt signaling upon reperfusion contributes to CKD-induced enlargement of infarct size.