Foam cell formation in atherosclerosis: HDL and macrophage reverse cholesterol transport

Shuai Zhang; L.R. Ritter; A.I. Ibragimov

doi:10.3934/proc.2013.2013.825

Article Contents

2013, Volume 2013: 825-835. Doi: 10.3934/proc.2013.2013.825 open access

This issue Previous Article Traveling wave solutions with mixed dispersal for spatially periodic Fisher-KPP equations Next Article Anosov diffeomorphisms

Foam cell formation in atherosclerosis: HDL and macrophage reverse cholesterol transport

1.
Southern Polytechnic State University, Marietta, GA 30060
2.
Southern Polytechnic State University, Marietta, GA 30060-2896
3.
Texas Tech University, Lubbock, TX 79409

Received: September 2012

Revised: December 2012

Published: November 2013

Abstract / Introduction Related Papers Cited by

Abstract

Macrophage derived foam cells are a major constituent of the fatty deposits characterizing the disease atherosclerosis. Foam cells are formed when certain immune cells (macrophages) take on oxidized low density lipoproteins through failed phagocytosis. High density lipoproteins (HDL) are known to have a number of anti-atherogenic effects. One of these stems from their ability to remove excess cellular cholesterol for processing in the liver---a process called reverse cholesterol transport (RCT). HDL perform macrophage RCT by binding to forming foam cells and removing excess lipids by efflux transporters.
We propose a model of foam cell formation accounting for macrophage RCT. This model is presented as a system of non-linear ordinary differential equations. Motivated by experimental observations regarding time scales for oxidation of lipids and MRCT, we impose a quasi-steady state assumption and analyze the resulting systems of equations. We focus on the existence and stability of equilibrium solutions as determined by the governing parameters with the results interpreted in terms of their potential bio-medical implications.

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Mathematics Subject Classification: Primary: 92B05, 92C50; Secondary: 34D20.

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