Mast cells are present in advanced human atherosclerotic plaques, where they are thought to exert multiple effects on their neighbouring cells and on the extracellular matrix of the plaque. Extensive efforts at delineating their role(s) in atherosclerotic plaques have unravelled mechanisms by which plaque mast cells may render advanced atherosclerotic plaques susceptible to erosion, rupture or intraplaque haemorrhage and so modulate their stability. In these mechanisms, the key effector molecules are mast-cell-derived neutral proteases and pro-inflammatory cytokines. These effector molecules are synthesized and stored in the cytoplasmic secretory granules of mast cells and, once the mast cells are activated to degranulate, are released into the microenvironment surrounding the activated mast cells. In the plaques, the key target cells are endothelial cells and smooth muscle cells and their pericellular matrices. In addition, the various components of the extracellular matrix of the plaques, notably collagen, are degraded when the released mast cell proteases activate matrix metalloproteinases in the plaques. By rendering the plaque susceptible to erosion, to rupture or to intraplaque haemorrhage, the mast cells may contribute to the onset of acute atherothrombotic complications of coronary atherosclerosis, such as myocardial infarction.

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