Fig. 1

The main therapeutic mechanisms of growth factors in ischemic vascular disease. The mechanism of HGF is mediated through its unique tyrosine kinase receptor (c-Met), which could drive intracellular signaling pathways (including the RAS‐MAPK, PI3K‐protein kinase B, and mTOR pathways). FGF regulates biological functions including cell proliferation, survival, migration, and differentiation by binding and activating FGF receptors via the RAS/MAPK pathway. PDGF gets involved in IVD through the PI3K pathway, the RAS pathway, and the PLC pathway. The induction of endothelial cells called tip, stem, and finger osteoblasts through interactions between VEGF and its receptor (VEGFR1-3) and between Notch and Delta-like nick ligands is essential for the regulation of angiogenesis. c-Met: cellular-mesenchymal epithelial transition factor; DAG: diacylglycerol; FGF: fibroblast growth factor; FGFR: fibroblast growth factor receptor; GEF: GMP exchange factor; HGF: hepatocyte growth factor; IP₃: inositol triphosphate; IVD: ischemic vascular disease; MAPK: mitogen-activated protein kinase; mTOR: mammalian target of rapamycin; PDGF: platelet-derived growth factor; PDGFR: platelet-derived growth factor receptor; PLC: phospholipase C; PKC: protein kinase C; PI3K: phosphatidylinositide 3-kinases; RAS: rat sarcoma; VEGF: vascular endothelial growth factor; VEGFR: vascular endothelial growth factor receptor. The figure was created by Figdraw (https://www.figdraw.com/)