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Front. Immunol. | doi: 10.3389/fimmu.2019.02505

Platelets as modulators of cerebral ischemia/reperfusion injury

 David Stegner1, 2, Vanessa Klaus1 and Bernhard Nieswandt1, 3*
  • 1Institute of Experimental Biomedicine, University Hospital of Würzburg, Germany
  • 2Julius Maximilian University of Würzburg, Germany
  • 3Rudolf Virchow Zentrum für experimentelle Biomedizin, Universität Würzburg, Germany

Ischemic stroke is among the leading causes of disability and death worldwide. In acute ischemic stroke, the rapid recanalization of occluded cranial vessels is the primary therapeutic aim. However, experimental data (obtained using mostly the transient middle cerebral artery occlusion model) indicates that progressive stroke can still develop despite successful recanalization, a process termed “reperfusion injury”. Mounting experimental evidence suggests that platelets and T cells contribute to cerebral ischemia/reperfusion injury, and ischemic stroke is increasingly considered a thrombo-inflammatory disease. The interaction of von Willebrand factor and its receptor on the platelet surface, glycoprotein Ib, as well as many activatory platelet receptors and platelet degranulation contribute to secondary infarct growth in this setting. In contrast, interference with GPIIb/IIIa-dependent platelet aggregation and thrombus formation does not improve the outcome of acute brain ischemia but dramatically increases the susceptibility to intracranial hemorrhage. Here, we summarize the current understanding of the mechanisms and the potential translational impact of platelet contributions to cerebral ischemia/reperfusion injury.

Keywords: Thrombo-inflammation, ischemic stroke, Platelet, Glycoprotein Ibα, platelet degranulation

Received: 31 Jul 2019; Accepted: 07 Oct 2019.

Copyright: © 2019 Stegner, Klaus and Nieswandt. 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.

* Correspondence: Prof. Bernhard Nieswandt, Institute of Experimental Biomedicine, University Hospital of Würzburg, Würzburg, 97080, Bavaria, Germany, bernhard.nieswandt@virchow.uni-wuerzburg.de