RT Journal Article
SR Electronic
T1 Biomechanical thrombosis: the dark side of force and dawn of mechano-medicine
JF Stroke and Vascular Neurology
JO Stroke Vasc Neurol Stroke Vasc Neurol
FD BMJ Publishing Group Ltd
SP svn-2019-000302
DO 10.1136/svn-2019-000302
A1 Chen, Yunfeng
A1 Ju, Lining Arnold
YR 2019
UL http://svn.bmj.com/content/early/2020/01/24/svn-2019-000302.abstract
AB 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’ .