One of the earliest events in the formation of an atherosclerotic lesion is the adherence of circulating monocytes to the vascular endothelium, through which they then gain entry to the sub-intimal tissue. This early lesion subsequently evolves over a number of years to form an atherosclerotic plaque, through the migration and proliferation of cells, the accumulation of lipid in the vessel wall and through the extensive deposition and modification of a connective tissue matrix. Pathological studies have described a wide spectrum of structural architecture in atherosclerotic plaques which suggests that, with time, the vascular connective tissue matrix is extensively modified during atherogenesis. This process of vascular connective tissue remodelling, where matrix macromolecules are both deposited and degraded, is controlled by a complex network of cell-cell and cell-matrix interactions, involving the secretion of a wide variety of growth factors and cytokines and chemokines.