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. 2022 May 26;44(1):881–892. doi: 10.1080/0886022X.2022.2079528

Figure 1.

Figure 1.

Pro-fibrotic effects of VEGF in chronic kidney disease. VEGF promotes the expression of VCAM-1, ICAM-1, and E-selectin through activation of the NF-κB signaling pathway. Persistent ER stress can initiate CHOP and caspase-12 apoptosis signaling pathway via three UPR branches: PERK-eIF2α-ATF4, IRE1, and ATF6 signaling pathways, eventually resulting in renal fibrosis. In turn, PERK also stimulates VEGF/VEGFR system. VEGF synergizes with PTHrP, TGF-β, and EGF in activating ERK1/2, thus promoting EMT that is related to renal fibrosis. (Abbreviations: VEGF, vascular endothelial growth factor; VCAM-1, vascular cell adhesion molecule-1; ICAM-1, intercellular adhesion molecule-1; ER, endoplasmic reticulum; UPR, unfolded protein response; VEGFR, vascular endothelial growth factor receptor; PTHrP, parathyroid hormone-related protein; TGF-β, transforming growth factor-β; EGF, epidermal growth factor; EMT, epithelial-to-mesenchymal transition; ZO-1, zonula occludens-1; α-SMA, α smooth muscle actin).