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Neurology 88 , 10971098 (2017)

It has been reported that promoting the phosphorylation of AKT can increase the expression of endothelial nitric oxide synthase in vascular endothelial cells, increase nitric oxide release, and protect against myocardial ischemia and reperfusion injury, while also reducing oxidative stress and protecting the myocardial mitochondria (49)

Activation of PI3K phosphorylates phosphatidylinositol 4,5-bisphosphate (PIP2) to form phosphatidylinositol 3,4,5-trisphosphate (PIP3), which then phosphorylates the serine-threonine kinase AKT, activating mTORC1 [66]