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. 2022 Jun 8;117(1):30. doi: 10.1007/s00395-022-00937-4

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© The Author(s) 2022

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 5 — Summary of endothelial ACKR3 in atherosclerosis. Graphical summary of EC-ACKR3-mediated processes (created with BioRender.com). Deficiency of ACKR3 in arterial endothelial cells leads to decreased atherosclerotic lesion sizes concomitant with decreased endothelial-immune cell adhesion. Endothelial ACKR3 silencing leads to downregulation of adhesion molecules and phosphorylated ERK1/2, Akt and NF-kB p65, which are inflammatory pathways involved in cell adhesion. Meanwhile, PPAR-γ, which suppresses NF-kB, is upregulated