A major hypothesis of atherogenesis ascribes endothelial damage as a causation of intimai proliferation which may, in turn, be a progenitor of arteriosclerosis. This hypothesis appears substantiated by experimental evidence varying from immunologic to mechanical damage of endothelium as a means of inducing both diffuse and focal intimai proliferation. There appears, in addition, other influences exerted by endothelial cells on the pathophysiology of intimai thickening. During intimai healing after wide spread endothelial denudation by an intraarterial balloon catheter, endothelial regrowth seems to promote regression of intimai thickening. It is not clear if this diminution of thickness is due to reduction in cells, extracellular material, or both. However, diminution of intimai thickening is not a feature of the healing process in the presence of hyperlipidemia. With widespread de-endothelialization, as described above, areas beneath regenerating endothelium are much thicker, and show a marked predisposition for the accumulation of lipid into the underlying already thickened intima. What physiologic or metabolic influences are exerted by the endothelium under these circumstances are unclear, but, the presence of endothelium may be a highly significant factor in the natural history of intimai proliferation and atherogenesis.