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. 2020 Sep 4;13:120. doi: 10.1186/s13045-020-00954-7

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© The Author(s) 2020

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/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 8 — Summary schemes illustrating SARS-CoV-2 activates platelets and enhances thrombosis in COVID-19. Global schema illustrating SARS-CoV-2 from alveolus binds and activates platelets, which enhances thrombosis formation and inflammatory reaction in capillaries, and subsequently contributes to development of disseminated intravascular coagulation and acute respiratory distress syndrome. SARS-CoV-2 Spike protein binds to ACE2 and phosphorylates ACE2, leading to MAPK signaling activation (phosphorylation of Erk, p-38, and JNK) and subsequent platelet activation, coagulation factors release, and inflammatory cytokines secretion. Interaction between SARS-CoV-2 Spike protein and platelet ACE2 confers the platelet activation, which is suppressed by the recombinant human ACE2 protein and anti-Spike monoclonal antibody (central illustration)