Welcome to our page dedicated to the results on mathematical modeling of atherosclerosis. Here, you will find brief information and some insights on research findings with the references for further reading. This list will be gradually completed and the readers will be informed about added results.
The level of LDL determines initiation of atherosclerosis
A simplest model of atherosclerosis represents a system of two ordinary differential equations for the concentrations of inflammatory cytokines and macrophages. Their positive feedback leads to the emergence of self-amplifying chronic inflammation. This process is launched by LDL cholesterol. If its concentration is low enough, then the desease-free stationary point is globally asymptotically stable, and atherosclerosis does not develop. If the LDL concentration exceed some critical value, then the desease-free point becomes unstable, while another stationary point appear and becomes stable. The desease will necessarily develop for any small perturbation which are always present in real life. Finally, for the interemediate cholesterol level, both points (desease free and endemic) are stable. Atherosclerosis will develop if the initial perturbation (inflammation, endothelial dysfunction) is large enough.
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