A mathematical model of atherogenesis as an inflammatory response

We construct a mathematical model of the early formation of an atherosclerotic lesion based on a simplification of Russell Ross' paradigm of atherosclerosis as a chronic inflammatory response. Atherosclerosis is a disease characterized by the accumulation of lipid-laden cells in the arterial wa...

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Bibliographic Details
Published in:Mathematical medicine and biology 2005-12, Vol.22 (4), p.305-333
Main Authors: Ibragimov, A. I., McNeal, C. J., Ritter, L. R., Walton, J. R.
Format: Article
Language:English
Subjects:
aggregation
atherogenesis
atherosclerosis
Atherosclerosis - etiology
Atherosclerosis - immunology
chemotaxis
Chemotaxis - physiology
chemotaxis equations
Humans
Inflammation - etiology
Inflammation - immunology
lesion progression
Mathematics
Models, Cardiovascular
Nonlinear Dynamics
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Summary:We construct a mathematical model of the early formation of an atherosclerotic lesion based on a simplification of Russell Ross' paradigm of atherosclerosis as a chronic inflammatory response. Atherosclerosis is a disease characterized by the accumulation of lipid-laden cells in the arterial wall. This disease results in lesions within the artery that may grow into the lumen restricting blood flow and, in critical cases, can rupture causing complete, sudden occlusion of the artery resulting in heart attack, stroke and possibly death. It is now understood that when chemically modified low-density lipoproteins (LDL cholesterol) enter into the wall of the human artery, they can trigger an immune response mediated by biochem‐ical signals sent and received by immune and other cells indigenous to the vasculature. The presence of modified LDL can also corrupt the normal immune function triggering further immune response and ultimately chronic inflammation. In the construction of our mathematical model, we focus on the inflammatory component of the pathogenesis of cardiovascular disease (CVD). Because this study centres on the interplay between chemical and cellular species in the human artery and bloodstream, we employ a model of chemotaxis first given by E. F. Keller and Lee Segel in 1970 and present our model as a coupled system of non-linear reaction diffusion equations describing the state of the various species involved in the disease process. We perform numerical simulations demonstrating that our model captures certain observed features of CVD such as the localization of immune cells, the build-up of lipids and debris and the isolation of a lesion by smooth muscle cells.
ISSN:1477-8599
1477-8602
DOI:10.1093/imammb/dqi011