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. 2021 Dec 22;12:787541. doi: 10.3389/fphar.2021.787541

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Copyright © 2021 Botts, Fish and Howe.

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 vascular endothelium directs site-specificity for plaque development and governs plaque progression. Both atheroprotective and atherogenic mechanisms are operative in endothelial cells (ECs) exposed to disturbed flow. EC-derived extracellular vesicles (EVs) mediate atheroprotective and atherogenic intercellular communication among ECs and between ECs and other immune and non-immune cell populations. Endothelial-to-mesenchymal transition (EndMT) contributes to the atherosclerotic disease process but may also maintain plaque stability.* ANXA2, annexin A2; ARHGAP18, Rho GTPase activating protein 18; COMP, cartilage oligomeric matrix protein; DNMT1, DNA methyltransferase 1; ERK5, extracellular signal-regulated kinase 5; HMGB1/2, high mobility group box protein 1/2; ID1, inhibitor of DNA binding 1; IL-1β, interleukin 1 beta; oxLDL, oxidized low-density lipoprotein; PLXND1, plexin D1; PRKAA1, protein kinase AMP-activated catalytic subunit alpha 1; SIRT1, sirtuin 1; SMC, smooth muscle cell; TGF-β, transforming growth factor beta; YAP, yes-associated protein; ZBTB46, zinc finger and BTB domain-containing protein 46.