Speaker
Description
Atherosclerosis is a disease driven by cholesterol accumulation within the arterial wall and involving coupled interactions between lipid transport and inflammation. Despite being a leading cause of cardiovascular disease, the spatial and stochastic mechanisms underlying plaque formation remain incompletely understood. To address this, we developed a hybrid continuum-discrete model of atherosclerotic plaque formation using the cell-based modelling framework Chaste. Our model incorporates feedback between lipid accumulation, cell death, and inflammatory chemokine production. We treat macrophages as discrete agents whose behaviour depends on the spatio-temporal distribution of lipoproteins, lipids, and the chemokine CCL2, whose dynamics are determined by a system of reaction-diffusion equations. The model is suitable for exploration of how cell-level processes influence local lipid and immune cell accumulation in early plaque development. Ongoing work focuses on exploring the model dynamics across parameter regimes.
