Inflame my plaque (inflammation and atherosclerosis)

Monocytes are a key cell type responsible for the generation of atherosclerosis. Monocytes/macrophages also play key roles in plaque growth and plaque instability. In contrast, recent research has demonstrated that macrophages can also suppress inflammation and promote healing and fibrosis. Some of this complexity relates to the presence of different macrophage subtypes that are induced and activated by different stimuli within the plaque. Macrophage functions include lipid uptake and oxidation with resultant foam cell formation, release of pro or anti-inflammatory cytokines, phagocytosis of dead macrophage and vessel wall cells, release of destructive enzymes such as matrix metalloproteinases, and presentation of antigen to immune cells. Each of these functions is likely to be occurring simultaneously in different subtypes within the complex environment of the plaque. While selective manipulation of monocytes/macrophages has clearly demonstrated their proatherogenic role in early plaque development, their role in advanced plaques has been more difficult to elucidate. Nonetheless, switching of a proinflammatory to an anti-inflammatory/reparative phenotype represents an attractive target for therapeutics in atherosclerosis. Heart Metab; 2013;60:5–8