['The activation of hepatic stellate cells (HSCs) is a key event in fibrotic pathogenesis. However, the mechanism involving activation of HSCs in chronic schistosomiasis is not entirely clear.', 'Human HSC LX-2 and human umbilical vein endothelial cells (ECs) were cultured with Schistosoma japonicum (S. japonicum) antigens (SA) in vitro. Fibrosis-associated genes and cell proliferation were analyzed. HSCs were isolated from mice of chronic schistosomiasis with or without praziquantel (PZQ) treatment, followed by the microarray analysis for the liver fibrosis-associated pathways.', 'Although SA inhibited the activation and proliferation of HSCs, it induced the EC proliferation and vascular endothelial growth factor-a (VEGF) production. VEGF significantly increased the proliferation of HSCs and up-regulated the expression of collagen and smooth muscle actin (α-SMA). For in vivo study, we found several fibrosis-associated pathways were involved in the HSCs during the reversal of liver fibrosis caused by schistosomiasis, including VEGF, PDGF, TNF and ET-1 pathways. The Ingenuity Pathway Analysis showed that VEGF directly regulated several pro-fibrotic and immune cytokine genes in HSCs, including integrin, fibronectin, IFN-γ, IL-6 and IL-10.'] Does vascular endothelial growth factor promote the activation of hepatic stellate cells in chronic schistosomiasis?