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Review
Biomechanical thrombosis: the dark side of force and dawn of mechano-medicine
  1. Yunfeng Chen1,
  2. Lining Arnold Ju2
  1. 1 Molecular Medicine, Scripps Research Institute, La Jolla, California, USA
  2. 2 School of Biomedical Engineering, Heart Research Institute and Charles Perkins Centre, The University of Sydney, Camperdown, New South Wales, Australia
  1. Correspondence to Dr Yunfeng Chen; cheny{at}scripps.edu; Dr Lining Arnold Ju; arnold.ju{at}sydney.edu.au

Abstract

Arterial thrombosis is in part contributed by excessive platelet aggregation, which can lead to blood clotting and subsequent heart attack and stroke. Platelets are sensitive to the haemodynamic environment. Rapid haemodynamcis and disturbed blood flow, which occur in vessels with growing thrombi and atherosclerotic plaques or is caused by medical device implantation and intervention, promotes platelet aggregation and thrombus formation. In such situations, conventional antiplatelet drugs often have suboptimal efficacy and a serious side effect of excessive bleeding. Investigating the mechanisms of platelet biomechanical activation provides insights distinct from the classic views of agonist-stimulated platelet thrombus formation. In this work, we review the recent discoveries underlying haemodynamic force-reinforced platelet binding and mechanosensing primarily mediated by three platelet receptors: glycoprotein Ib (GPIb), glycoprotein IIb/IIIa (GPIIb/IIIa) and glycoprotein VI (GPVI), and their implications for development of antithrombotic ‘mechano-medicine’ .

  • Blood Flow
  • Stenosis
  • Platelets
  • Stroke
  • Vessel Wall
http://creativecommons.org/licenses/by-nc/4.0/

This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited, appropriate credit is given, any changes made indicated, and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/.

https://doi.org/10.1136/svn-2019-000302

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    Footnotes

    • YC and LAJ contributed equally.

    • Correction notice This article has been corrected since it was first published. Orcid iD for

      author Lining Arnold Ju has been added.

    • Contributors Both authors wrote the manuscript and made the table. YC drew the figures.

    • Funding This work was supported by grants from Sydney Research Accelerator (SOAR) prize (L.A.J.), The Royal College of Pathologists of Australasia Kanematsu research award (L.A.J.) and the Cardiac Society of Australia and New Zealand BAYER Young Investigator Research Grant (L.A.J.). We thank Zaverio Ruggeri, Yilong Wang, Liping Liu, Jing-fei Dong and Yi Qian for helpful discussion. Y.C. is a MERU (Medolago-Ruggeri) Foundation post-doctoral awardee. L.A.J. is an Australian Research Council DECRA fellow (DE190100609) and a National Heart Foundation Future Leader fellow (102532).

    • Competing interests None declared.

    • Patient consent for publication Not required.

    • Provenance and peer review Commissioned; internally peer reviewed.