Biomechanical thrombosis: the dark side of force and dawn of mechano-medicine.

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' .

• Authors: Yunfeng Chen, Lining Arnold Ju
• Journal: Stroke and vascular neurology (Stroke Vasc Neurol) Vol. 5 Issue 2 Pg. 185-197 (06 2020) ISSN: 2059-8696 [Electronic] England
• PMID: 32606086 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)
• Copyright: © Author(s) (or their employer(s)) 2020. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.

Chemical References

• Fibrinolytic Agents
• Platelet Aggregation Inhibitors
• Platelet Glycoprotein GPIIb-IIIa Complex
• Platelet Glycoprotein GPIb-IX Complex
• Platelet Membrane Glycoproteins
• adhesion receptor
• platelet membrane glycoprotein VI

Topics

• Animals
• Arterial Occlusive Diseases (blood, drug therapy, physiopathology)
• Blood Coagulation (drug effects)
• Blood Platelets (drug effects, metabolism)
• Fibrinolytic Agents (adverse effects, therapeutic use)
• Hemodynamics
• Humans
• Mechanotransduction, Cellular (drug effects)
• Molecular Targeted Therapy
• Platelet Activation (drug effects)
• Platelet Aggregation Inhibitors (adverse effects, therapeutic use)
• Platelet Glycoprotein GPIIb-IIIa Complex (antagonists & inhibitors, metabolism)
• Platelet Glycoprotein GPIb-IX Complex (antagonists & inhibitors, metabolism)
• Platelet Membrane Glycoproteins (antagonists & inhibitors, metabolism)
• Stress, Mechanical
• Thrombosis (blood, diagnosis, drug therapy)