• Corpus ID: 248665603

A lipid-structured mathematical model of atherosclerosis with macrophage proliferation

@inproceedings{Chambers2022ALM,
  title={A lipid-structured mathematical model of atherosclerosis with macrophage proliferation},
  author={Keith L Chambers and Michael G. Watson and Mary R. Myerscough},
  year={2022}
}
We extend the lipid-structured model for atherosclerotic plaque development of Ford et al (2019) to account for macrophage proliferation. Proliferation is modelled as a non-local decrease in the lipid structural variable that is similar to the treatment of cell division in size-structured models (e.g. Efendiev et al (2018)). Steady state analysis indicates that proliferation assists in reducing eventual necrotic core size and acts to spread the lipid load of the macrophage population amongst… 
[PDF] Semantic Reader
2 Citations
Background Citations
1
Methods Citations
1

Figures and Tables from this paper

2 Citations

A new lipid-structured model to investigate the opposing effects of LDL and HDL on atherosclerotic plaque macrophages.

Macrophage Anti-inflammatory Behaviour in a Multiphase Model of Atherosclerotic Plaque Development

A free boundary multiphase model for early atherosclerotic plaques is developed and used to investigate the effects of impaired macrophage anti-inflammatory behaviour on plaque structure and growth, and it is found that high rates of cell death relative to efferocytic uptake results in a plaque populated mostly by dead cells.

36 References

A lipid-structured model for macrophage populations in atherosclerotic plaques

A system of partial integro-differential equations that model lipid accumulation by macrophages, including generating apoptotic cells and a necrotic core is constructed, finding the qualitative form of lipid distribution across the macrophage population and showing that high lipid loads can occur in the absence of LDL ingestion.

Modelling Preferential Phagocytosis in Atherosclerosis: Delineating Timescales in Plaque Development

A simple ODE model for lipid dynamics that includes macrophage preference for ingesting apoptotic material and modified low-density lipoproteins (modLDL) over ingesting necrotic material is proposed, showing that if the necrosis rate is small then the necrotics core in the model plaque may continue to develop slowly even when the lipid levels in plaque macrophages, apoptoticmaterial and modLDL appear to have reached equilibrium.

Macrophages in atherosclerosis: a dynamic balance

Recently identified pro- and anti-inflammatory pathways that link lipid and inflammation biology with the retention of macrophages in plaques, as well as factors that have the potential to promote their egress from these sites are summarized.

Monocyte Recruitment, Specification, and Function in Atherosclerosis

Recent advances regarding the role of monocyte and macrophage dynamics in atherosclerotic disease are highlighted and gaps in knowledge are identified that the hope will allow for advancing therapeutic treatment or prevention strategies for cardiovascular disease.

Mathematical modelling of the atherosclerotic plaque formation

This article provides a mathematical model in which the lesion appears in the area of lower shear stress, and considers that the inflammatory process starts with the penetration of Low Density Lipoproteins cholesterol in the intima.

Bifurcation and dynamics in a mathematical model of early atherosclerosis

A mathematical model describing the primary mechanisms that drive the early stages of atherosclerosis involves the interactions between modified low density lipoprotein, monocytes/macrophages, cytokines and foam cells and shows the existence of a fold bifurcation when the flux of LDL from the blood is sufficiently high.

Local proliferation dominates lesional macrophage accumulation in atherosclerosis

Macrophage proliferation is revealed as a key event in atherosclerosis and macrophage self-renewal is identified as a therapeutic target for cardiovascular disease.

Nonlinear dynamics of early atherosclerotic plaque formation may determine the efficacy of high density lipoproteins (HDL) in plaque regression

The model predicts that when HDL influx into a well-established plaque with large numbers of foam cells is increased, the plaque may not regress but may continue to grow at a slower rate, while the intrinsic dynamics of reverse cholesterol transport by HDL are important in determining the success of HDL raising in promoting plaque regression.

Macrophage Phenotype and Function in Different Stages of Atherosclerosis.

Recent advances in the understanding of lesional macrophage phenotype and function in different stages of atherosclerosis are discussed.

Quantification of Monocyte Transmigration and Foam Cell Formation from Individuals with Chronic Inflammatory Conditions.

A protocol in which monocytes isolated from patient blood transmigrate across human endothelial cells into a type 1 collagen matrix, and their propensity to mature into foam cells in the presence or absence of exogenous lipid is measured is described.