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DOI: 10.1055/a-2676-4451
Physical and Mechanobiological Basis of Biological Functions of Platelets
Funding This work was supported by Cross-ministerial Strategic Innovation Promotion Program (SIP) on “Integrated Health Care System” Grant Number JPJ012425, and by the grant from Fukuda Memorial Foundation, and a grant from the Nakatani Foundation for Advancement of Measuring Technologies in Biomedical Engineering, and Suzuken Memorial Foundation, and MEXT/JSPS KAKENHI Grant-in-Aid (Grant Number 19H03661), and AMED (Grant Numbers A368TS and A447TR).

Abstract
Platelets play a unique role in thrombosis and hemostasis. Historical research has revealed biological mechanisms underlying various platelet functions. However, unraveling the complex mechanisms underlying various platelet functions is challenging. Recent progress in high-performance computer has enabled an understanding of the complex biological functions of platelets through combinations of basic principles of physics, such as Newton's laws of motion, fluid mechanics, and mechanobiology. Platelets are blood cells with diameters of 2 to 5 µm. They lack nuclei but contain organelles such as mitochondria. Platelets promptly adhere to the sites of endothelial damage for hemostasis. Adherent platelets are activated to allow plasma ligands of fibrinogen and von Willebrand factor (VWF) to bind stably to them. They also enhance local coagulant activity through their procoagulant activity. The specific biological functions of platelets are mediated by dynamic structural changes in their membrane proteins. Even lipids and proteins that mediate the specific functions of platelets are constructed from atoms following basic physical rules, such as Newton's laws of motion. Thus, the various biological functions of platelets can be constructed from physical principles, starting with the movement of atoms. Here, various complex biological functions of platelets were constructed using mathematical models and simple physical principles. This framework may help explain the complex pathophysiological mechanisms underlying the VWF–platelet interaction in both healthy and diseased conditions. Detailed quantitative biological experiments confirmed the validity of these mathematical models. The future direction of constructive “theoretical medicine and biology,” starting from atomic movements, is expected to follow.
Keywords
platelets - adhesion - von Willebrand factor - GPIbα - GPIIb/IIIa - molecular dynamic simulation - high-performance computerPublikationsverlauf
Eingereicht: 31. März 2025
Angenommen: 18. Juli 2025
Accepted Manuscript online:
05. August 2025
Artikel online veröffentlicht:
20. August 2025
© 2025. The Author(s). This is an open access article published by Thieme under the terms of the Creative Commons Attribution License, permitting unrestricted use, distribution, and reproduction so long as the original work is properly cited. (https://creativecommons.org/licenses/by/4.0/)
Georg Thieme Verlag KG
Oswald-Hesse-Straße 50, 70469 Stuttgart, Germany
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