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. 2021 Mar 9;12:632378. doi: 10.3389/fphar.2021.632378

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Copyright © 2021 Zhao, Qian, Sun, Shen, Cai, Li and Wang.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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The PI3K signaling pathway and related target drugs in endothelial cells. The PI3K signaling pathway affects three main factors in endothelial cells: 1. Survival and apoptosis. ① Kaempferol enhances autophagy by inhibiting PI3K/Akt/mTOR and inhibiting apoptosis. ② Scutellarin exerts antiapoptotic effects through PI3K/Akt/FOXO3a. 2. Inflammation. ③ ApoM-S1P/S1PR2 activates PI3K/Akt, which suppresses ox-LDL-induced inflammation. ④FSH/FSHR activate PI3K/Akt/mTOR/NF-κB, increase ICAM-1 expression and promote monocyte-endothelial cell adhesion 3. Oxidation. ⑤ Klotho, XJP can downregulate the expression of LOX-1 and by PI3K/Akt/eNOS/NO-mediated inhibition of the increase in ROS, resisting apoptosis. ⑥Andrographolide increases GSH and HO-1 and inhibits TNF-α-induced ROS production through PI3K/Akt/Nrf2 and PI3K/Akt/AP-1-mediated upregulation of expression. Lunasin increases HO-1 through PI3K/Akt/Nrf2.