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. 2019 Jun 6;10:1260. doi: 10.3389/fimmu.2019.01260

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Copyright © 2019 Schanze, Bode and Duerschmied.

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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Overview of relevant platelet derived mediators and their influence on myocardial ischemia/reperfusion injury (IRI). Endothelial damage caused by IRI leads to activation of platelets. This is accompanied by upregulation of surface proteins and the release of immunomodulatory contents that influence the progression of IRI via different mechanisms. Platelet receptors that are involved in IRI aggravation are glycoprotein (GP) IIb/IIIa, GPVI and P2Y12. Additionally, platelet membrane proteins, such as sodium-hyodrogen-exchanger 1 (NHE1), Gαq, Gαi2, and P-selectin, or secretable factors, e.g., reactive oxygen species (ROS) and serotonin, worsen the cardiac outcome after myocardial infarction. Cardioprotective effects are for example exerted by platelet-derived sphingosine-1-phosphate (S1P), low concentrations of platelet activating factor (PAF) and transforming growth factor beta 1(TGFβ1).