AKT1 and Cerebral ischemia: IPostC can reduce ischemia-reperfusion injury by regulating a variety of endogenous neuroprotective mechanisms, including reducing ROS production, alleviating inflammatory and cerebral ischemia-reperfusion injury by activating autophagy, inhibiting inflammation of local injured tissues, endoplasmic reticulum stress, and neuronal apoptosis, improving cerebral blood supply, and regulating phosphorylation of the MAPK, protein kinase C, Notch, and PI3K/Akt pathways [58,59].