Disturbances in the integrity of the arterial endothelium are considered to be a primary event in the pathogenesis of atherosclerosis. Platelets do not adhere to the intact endothelium but with removal of the endothelium, a thrombotic response to the exposed thrombotic subendothelium occurs. With time, proliferation of smooth muscle cells occurs in the inner-most part of the media beneath the thrombus, and the proliferated smooth muscle cells migrate beyond the internal elastic lamina to invade the thrombus and organize it. A growth factor released from activated platelets (PDGF) stimulates smooth muscle cell proliferation. At the same time, the endothelium, adjacent to the thrombus, proliferates and covers the organizing thrombus from its margin. Thus, localized flat or raised intimal thickenings are formed from organization of mural thrombus or repair of intimal injury. There is much evidence that the release of platelet constituents can damage the vessel wall. Our study clearly demonstrated that material released from situ platelet-rich mural thrombi into the arterial circulation can cause endothelial damage and promote the proliferation of smooth muscle cells in the intima, downstream, and in remote segments of the arterial wall, without apparent endothelial denudation. PDGF, together with other growth factors, is also considered to be involved in smooth muscle cell proliferation in this case.