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These events trigger vascular constriction and activate inflammatory pathways, together promoting atheromatous plaque development. This review integrates emerging concepts in the immune cascade, detailing how recruited immune cells such as macrophages, T cells, B cells, dendritic cells (DCs), and neutrophils interact to sustain inflammation within developing plaques, as revealed by single-cell omics approaches. In addition, we discuss novel ideas, such as phenotypic switching of vascular smooth muscle cells into macrophage-like foam cells and the systemic effects of clonal haematopoiesis. 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