Visfatin exerts angiogenic effects on human umbilical vein endothelial cells through the mTOR signaling pathway

► Visfatin-induced angiogenesis requires mTOR and GSK3β signaling downstream of the PI3-kinase/Akt signaling pathway. ► Activation of mTOR inactivates GSK3β, which promotes the nuclear translocation of β-catenin, thereby increasing the expression of cyclin D1 and VEGF. ► β-Catenin knockdown attenuates visfatin-induced endothelial cell proliferation and capillary tube formation. ► Collectively, these results show that the activation of mTOR and the inactivation of GSK3β play key roles in visfatin-induced angiogenesis.