Resveratrol and angiogenesis

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Angiogenesis is important in atherosclerosis where EC migration, proliferation are essential events in this process. Vascular endothelial growth factor (VEGF) co-localizes with endothelial cells, macrophages and SMC in atherosclerotic plaques [101]. Resveratrol inhibits VEGF-induced angiogenesis by abrogating VEGF-mediated tyrosine phosphorylation of vascular-cadherin and its complex partner, b-catenin [102]. The inhibition of VEGF-induced angiogenesis is mediated by the disruption of ROS-dependent Src kinase activation and the subsequent VE-cadherin tyrosine phosphorylation. Resveratrol can also reduce VEGF by its action on NADPH oxidase [27, 28] which regulates the induction of VEGF expression [103] and the VEGF-induced angiogenesis [104]. VEGF expression can be also regulated by pro-apoptotic factors such as AngII, which may be accumulated in response to ECs damage. Consequently to its effect on Ang II, resveratrol can inhibit Ang II-mediated VEGF expression [86]. Furthermore, it inhibits both the FGF (fibroblast growth factor) receptor- and the VEGF receptor-mediated EC responses [105].