Modeling of the early stage of atherosclerosis with emphasis on the regulation of the endothelial permeability
In this paper, we develop a mathematical model for the early stage of atherosclerosis, as a chronic inflammatory disease. It includes also processes that are relevant for the ”thickening” of the vessel walls, and prepares a more complete model including also the later stages of atherosclerosis. The...
Gespeichert in:
| Hauptverfasser: | , , , |
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| Dokumenttyp: | Article (Journal) |
| Sprache: | Englisch |
| Veröffentlicht: |
04 April 2020
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| In: |
Journal of theoretical biology
Year: 2020, Jahrgang: 496 |
| ISSN: | 1095-8541 |
| DOI: | 10.1016/j.jtbi.2020.110229 |
| Online-Zugang: | Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1016/j.jtbi.2020.110229 Verlag, lizenzpflichtig, Volltext: http://www.sciencedirect.com/science/article/pii/S0022519320300849 
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| Verfasserangaben: | Telma Silva, Willi Jäger, Maria Neuss-Radu, Adélia Sequeira |
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| 520 | |a In this paper, we develop a mathematical model for the early stage of atherosclerosis, as a chronic inflammatory disease. It includes also processes that are relevant for the ”thickening” of the vessel walls, and prepares a more complete model including also the later stages of atherosclerosis. The model consists of partial differential equations: Navier-Stokes equations modeling blood flow, Biot equations modeling the fluid flow inside the poroelastic vessel wall, and convection/chemotaxis-reaction-diffusion equations modeling transport, signaling and interaction processes initiating inflammation and atherosclerosis. The main innovations of this model are: a) quantifying the endothelial permeability to low-density-lipoproteins (LDL) and to the monocytes as a function of WSS, cytokines and LDL on the endothelial surface; b) transport of monocytes on the endothelial surface, mimicking the monocytes adhesion and rolling; c) the monocytes influx in the lumen, as a function of factor increasing monocytopoiesis; d) coupling between Navier-Stokes system, Biot system and convection/chemotaxis-reaction-diffusion equations. Numerical simulations of a simplified model were performed in an idealized two-dimensional geometry in order to investigate the dynamics of endothelial permeability, and the growth and spread of immune cells populations and their dependence in particular on low-density-lipoprotein and wall-shear stress. | ||
| 650 | 4 | |a Atherosclerosis | |
| 650 | 4 | |a Early inflammation | |
| 650 | 4 | |a Endothelial permeability | |
| 650 | 4 | |a Immune cells dynamics | |
| 650 | 4 | |a Low-density-lipoprotein dynamics | |
| 650 | 4 | |a Mathematical modeling and simulations | |
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