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. 2018 Oct 12;9:1236. doi: 10.3389/fphys.2018.01236

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Copyright © 2018 Hu and Zhu.

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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Schematic representation of the role of Sema3E in atherosclerosis. (A) In the early stage of atherosclerosis, Sema3E and its receptor PlexinD1 are remarkably decreased in atherosclerotic plaques. Sema3E inhibits VSMC migration and proliferation by inactivating Rap1-AKT signaling pathways via binding to PlexinD1 in the process of neointimal formation. (B) Sema3E and its receptor PlexinD1 are remarkably increased in monocyte-macrophages of advanced atherosclerotic plaques. Sema3E inhibits the directional emigration of macrophages by disrupting the Rho GTPase signaling cascade and actin cytoskeleton reorganization via binding to PlexinD1, which promotes monocyte-macrophage retention, exacerbating atherosclerosis.