Theoretical modeling demonstrates how thrombin and fibrinogen ratios dictate fiber thickness and mesh architecture, indicating physical mechanisms governing clot density.
Fibrin polymerization is responsible for the formation of blood clots and is used in many biomedical applications. Considering polymerization as a dynamic phase transition, we constructed a scaling theory of fibrin networks formation. We show that in the transient state, protofibrils and branched clusters are self-assembled as a result of diffusion-controlled reactions with free fibrin monomers. The rate of reactions increases with initial concentrations of fibrinogen and thrombin. Protofibrils and clusters aggregate laterally, forming fibers, the elongation of which leads to their crosslinking to form a fibrin network. We calculated the network structure for different ratios of lag time and fibrinogen activation time. At a low ratio of fibrinogen and thrombin concentrations, sparse networks of thick and long fibers are formed, whereas at a high ratio, dense networks of thin and short fibers. The predicted concentration dependences of network parameters are in agreement with experimental data.
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Sergey Panyukov (2024) studied this question.
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