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. 2023 Mar 13;2(3):307–321. doi: 10.1038/s44161-023-00224-y

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© The Author(s) 2023

Open Access This 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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 7 — a, Representative en face images of Tie2^WT and Tie2^iΔAEC (n = 3 per group) aortas stained for Foxo1 (red) and DAPI (blue) (top). Scale bar, 20 μm. Quantification of nuclear versus cytoplasmic Foxo1 expression in the endothelial cells (dashed lines) (n = 3 independent mice per group; P = 0.0044) (bottom). Values show mean ± s.d. Statistical significance was determined using Student’s t-test (two-tailed, unpaired). b, Schematic showing a summary of the main results. GWAS analysis indicates that Tie2 activity is involved in human CAD via disruption of Tie–Akt signaling axis and via inhibition of Foxo1 nuclear localization and transcriptional activity. When Tie2 alone or the whole Tie1;Tie2 receptor complex is deleted from the aortic endothelium, VCAM1 expression is induced via Foxo1 transcriptional transactivation and blood leukocytes adhere to the aortic endothelium, which promotes atheroma formation. ECs, endothelial cells.

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