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. 2020 Mar 11;11:1315. doi: 10.1038/s41467-020-14958-x

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© The Author(s) 2020

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 During myocardial ischemia shear stress and hypoxia result in cleavage of Sema7a from the surface of erythrocytes as the main source of Sema7a within the vascular bed. b The released Sema7a then engages the Glycoprotein Ib receptor and activates platelets which then exposes the integrin receptors resulting in platelet–neutrophil complex formation (PNCs). c Activated platelets and PNCs migrate from the vasculature to the ischemic tissue which results in tissue injury and destruction.