Cooperative SIR dynamics as a model for spontaneous blood clot initiation

TL;DR

This paper introduces a minimal SIR-inspired model for spontaneous blood clotting, highlighting the importance of platelet heterogeneity and hyper-sensitive subpopulations in initiating collective activation, with qualitative experimental agreement.

Contribution

The study presents a novel minimal model for blood clot initiation that emphasizes the role of platelet sensitivity heterogeneity and hyper-sensitive subpopulations.

Findings

Small initial signals can trigger clotting with sufficient heterogeneity.

Hyper-sensitive platelets are crucial for propagating activation.

Model shows qualitative agreement with experimental data.

Abstract

Blood clotting is an important physiological process to suppress bleeding upon injury, but when it occurs inadvertently, it can cause thrombosis, which can lead to life threatening conditions. Hence, understanding the microscopic mechanistic factors for inadvertent, spontaneous blood clotting, in absence of a vessel breach, can help in predicting and adverting such conditions. Here, we present a minimal model -- reminiscent of the SIR model -- for the initiating stage of spontaneous blood clotting, the collective activation of blood platelets. This model predicts that in the presence of very small initial activation signals, macroscopic activation of the platelet population requires a sufficient degree of heterogeneity of platelet sensitivity. To propagate the activation signal and achieve collective activation of the bulk platelet population, it requires the presence of, possibly only few, hyper-sensitive platelets, but also a sufficient proportion of platelets with intermediate, yet higher-than-average sensitivity. A comparison with experimental results demonstrates a qualitative agreement for high platelet signalling activity.