The formation of the "early proliferative lesion" of arteriosclerosis is the result of a chronic interaction of endothelial cells, monocytes/macrophages, smooth muscle cells, and potentially other cells such as T-lymphocytes and platelets. The precise manner in which these cells ineract during the early stage of the disease is unclear. The initial mechanisms involved in the pathophysiological interaction of these cells in the presence of the clinically important risk factors remain to be determined and represent a major challenge for future research. As we learn more about the molecular mechanisms we will be able to develop new strategies of therapy to prevent the disease.
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