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HO1 overexpression augmented vascular endothelial growth factor (VEGF) production and VEGFmediated angiogenic activities by increasing proliferation, migration, the formation of tubes on Matrigel, and the outgrowth of capillaries from endothelial spheroids.121 The proangiogenic role of VEGF/Nrf2dependent pathway induced by Nrf2 activation was proved in rat gastric epithelial cells122 as well as glioma cells123 and pancreatic cancer cells.124 Nrf2 blockade inhibited hypoxiainduced activation of HIF1/VEGF signaling to suppress tumor angiogenesis, indicating a crosstalk mechanism between Nrf2 and HIF1 in angiogenesis.125 3.6

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