Abstract
The paradigm shift in cardiovascular biology has been the understanding that atherosclerosis involves not just a mechanical deposition of lipids in the vessel wall, but a dynamic process involving the inflammatory response with cellular infiltration and inflammatory mediator expression. Typical cellular elements that have been studied include endothelial cells, vascular smooth muscle, T lymphocyte and the macrophage. Recent data suggests a role for the human mast cell. The human mast cell is a tissuedwelling cell, typically perivascular in distribution. This multifunctional cell responds rapidly to challenge with the release of inflammatory mediators that can orchestrate an immune response and may have relevance to atherogenesis. Mast cells have been shown to modulate various aspects of cardiovascular disease such as atherogenesis (endothelial activation, cytokine generation and foam cell formation) as well as rupture of an unstable atheromatous plaque. Mast cell activation in the context of cardiovascular disease may occurby cognate cell-cell interactions (interactions with macrophages, T cells, endothelial cells or smooth muscle) or by non-cognate means (such as lipoproteins and other proatherogenic components). More studies are required in order to better understand the molecular role of mast cells in vascular inflammatory disease.