<p>Smooth muscle cells (SMCs) play a fundamental role in the development of atherosclerotic plaques. They ingest lipids in a similar way to monocyte-derived macrophages (MDMs) in the plaque. This can stimulate SMCs to undergo a phenotypic switch to a macrophage-like phenotype. We formulate an ordinary differential equation (ODE) model for the populations of SMCs, MDMs and smooth muscle cell-derived macrophages (SDMs) and the internalised lipid load in each population. We use this model to explore the effect on plaque fate of SMC phenotype switching. We find that when SMCs switch to a macrophage-like phenotype, there is an increase in the lipid quantity in the model plaque that is internalised inside cells. Additionally, removal of SMCs from the model plaque via phenotype switching reduces the number of SMCs in the fibrous cap, increases the lipid in the necrotic core, and increases plaque inflammation. These features are hallmarks of vulnerable plaques, whose rupture can cause heart attacks or strokes. When SDMs are highly proliferative or resistant to cell death, the model plaque becomes increasingly pathological. The model suggests that the switch of SMCs to a macrophage-like phenotype may drive the development of unstable and pathological plaques.</p>