Atherosclerotic lesions develop at the site of vascular endothelium damage, leading to up-regulation of vascular adhesion molecules (e.g. VCAM1, ICAM) and expression of monocyte chemoattractants [monocyte chemoattractant protein-1 (e.g. MCP-1/CCL2)]. Together, these facilitate leukocyte migration and adhesion. Smooth muscle cells (vSMCs) proliferate and migrate to the lesion, undergoing a defifferentiation from contractile to synthetic SMCs. Recent studies investigating SMC plasticity during atherosclerosis suggest that SMC phenotypic switching can contribute multiple cell-types within the lesion, including macrophage-like cells, foam-cell like cells, myofibroblast-like cells and mesenchymal stem cell like cells. In response to proatherogenic stimuli within the vessel wall, macrophages transform into lipid-laden foam cells which significantly contribute to lesion progression. T-cell activation and platelet adherence also occurs. Plaque rupture occurs in advanced lesions as a result of fibrous cap thinning. Created with BioRender.com.