ArticleMultiscale modeling & simulation : a SIAM interdisciplinary journal2020
A MATHEMATICAL MODEL OF PLATELET AGGREGATION IN AN EXTRAVASCULAR INJURY UNDER FLOW.
Article in Multiscale modeling & simulation : a SIAM interdisciplinary journal, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 1 citations in OpenAlex.
- Modeling the role of platelet-released polyphosphates in tissue factor-initiated coagulation under flow.Research and practice in thrombosis and haemostasis · 2026Article
- A three-dimensional shear dependent continuum model of platelet aggregation under flow.PLoS computational biology · 2026Article
- Platelet activation near point-like source of agonist: Experimental insights and computational model.PloS one · 2024Article
- A Multiscale Model for Shear-Mediated Platelet Adhesion Dynamics: Correlating In Silico with In Vitro Results.Annals of biomedical engineering · 2023Article
- Image Fusion and Stylization Processing Based on Multiscale Transformation and Convolutional Neural Network.Computational intelligence and neuroscience · 2022Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
Abstract
We present the first mathematical model of flow-mediated primary hemostasis in an extravascular injury which can track the process from initial deposition to occlusion. The model consists of a system of ordinary differential equations (ODEs) that describe platelet aggregation (adhesion and cohesion), soluble-agonist-dependent platelet activation, and the flow of blood through the injury. The formation of platelet aggregates increases resistance to flow through the injury, which is modeled using the Stokes-Brinkman equations. Data from analogous experimental (microfluidic flow) and partial differential equation models informed parameter values used in the ODE model description of platelet adhesion, cohesion, and activation. This model predicts injury occlusion under a range of flow and platelet activation conditions. Simulations testing the effects of shear and activation rates resulted in delayed occlusion and aggregate heterogeneity. These results validate our hypothesis that flow-mediated dilution of activating chemical adenosine diphosphate hinders aggregate development. This novel modeling framework can be extended to include more mechanisms of platelet activation as well as the addition of the biochemical reactions of coagulation, resulting in a computationally efficient high throughput screening tool of primary and secondary hemostasis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.