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. 2021 Apr 21;15:652647. doi: 10.3389/fncel.2021.652647

Figure 2.

Figure 2

The molecular mechanism of angiogenesis mediated by the PI3K/AKT pathway. PI3K signaling is activated by the endothelial growth factor receptor (EGFR), fibroblast growth factor receptor (FGFR), IL-6R, and Ang/Tie2 signaling molecules, leading to AKT activation. Activated AKT promotes the expression of Bad, which inhibits Bcl-CL/Bcl-2, thereby promoting the survival of pro-angiogenic cells. The mechanistic target of rapamycin (mTOR) is also activated by AKT and increases the level of HIF-1α, which can directly increase the expression of vascular endothelial growth factor (VEGF) or bind to HIF-1β in hypoxia conditions and transfer to the nucleus to promote the expressions of erythropoietin (EPO) and VEGF. Meanwhile, endothelial nitric oxide synthase (eNOS) activated by AKT promotes the production of NO, which protects vascular tone permeability. These potential mechanisms contribute to angiogenesis through the PI3K/AKT pathway.