Fig. 3. Major factors and signaling pathways of angiogenesis after cerebral ischemia. Ischemia or hypoxia resulting from cerebral ischemia increased VEGF expression by upregulating HIF-1α and 15-LO-1/15-HETE systems, and subsequently VEGF promoted pericyte coverage of ECs by increasing N-cadherin expression on brain capillaries.

NGF promoted angiogenesis by activating p-focal adhesion kinase (FAK) or PI3K/Akt signaling pathways after ischemic stroke, and similar pathways had also been found in TSLP and its receptor TSLPR. IL-1α, TNF-1α and SDF-1α also promoted angiogenesis by activating the expression of downstream genes through their receptors, respectively.