Sumiyoshi A, Asada Y, Kisanuki A, Hayashi T
First Department of Pathology, Miyazaki Medical College.
Nihon Rinsho. 1992 Feb;50(2):307-10.
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.
动脉内皮完整性的破坏被认为是动脉粥样硬化发病机制中的首要事件。血小板不会黏附于完整的内皮，但在内皮被去除后，会对暴露的血栓形成性内皮下层产生血栓形成反应。随着时间的推移，血栓下方中膜最内层会发生平滑肌细胞增殖，增殖的平滑肌细胞迁移至内弹力层之外，侵入血栓并使其机化。活化血小板释放的生长因子（血小板源性生长因子）刺激平滑肌细胞增殖。与此同时，与血栓相邻的内皮细胞增殖，从血栓边缘覆盖机化的血栓。因此，壁血栓机化或内膜损伤修复形成局部扁平或隆起的内膜增厚。有大量证据表明血小板成分的释放会损害血管壁。我们的研究清楚地表明，富含血小板的壁血栓原位释放到动脉循环中的物质可导致内皮损伤，并促进动脉壁下游及远端节段内膜平滑肌细胞的增殖，且无明显的内皮剥脱。在这种情况下，血小板源性生长因子与其他生长因子一起也被认为参与了平滑肌细胞的增殖。
