Yamashita Atsushi, Asada Yujiro
Department of Pathology, Faculty of Medicine, University of Miyazaki, 5200 Kihara, Kiyotake, Miyazaki 889-1692, Japan.
J Biomed Biotechnol. 2011;2011:424929. doi: 10.1155/2011/424929. Epub 2010 Dec 26.
Thrombus formation on a disrupted atherosclerotic plaque is a key event that leads to atherothrombosis. Because thrombus is induced by chemical or physical injury of normal arteries in most animal models of thrombosis, the mechanisms of thrombogenesis and thrombus growth in atherosclerotic vessels should be investigated in diseased arteries of appropriate models. Pathological findings of human atherothrombosis suggest that tissue factor, an initiator of the coagulation cascade, significantly affects enhanced platelet aggregation and fibrin formation after plaque disruption. We established a rabbit model of atherothrombosis based on human pathology in which differences in thrombus formation between normal and atherosclerotic arteries, factors contributing to thrombus growth, and mechanisms of plaque erosion can be investigated. Emerging transgenic and stem cell technologies should also provide an invaluable rabbit experimental model in the near future.
在破裂的动脉粥样硬化斑块上形成血栓是导致动脉粥样硬化血栓形成的关键事件。由于在大多数血栓形成动物模型中，血栓是由正常动脉的化学或物理损伤诱导的，因此应在合适模型的病变动脉中研究动脉粥样硬化血管中血栓形成和血栓生长的机制。人类动脉粥样硬化血栓形成的病理结果表明，凝血级联反应的启动因子组织因子在斑块破裂后对增强血小板聚集和纤维蛋白形成有显著影响。我们基于人类病理学建立了兔动脉粥样硬化血栓形成模型，在该模型中可以研究正常动脉和动脉粥样硬化动脉之间血栓形成的差异、促成血栓生长的因素以及斑块侵蚀的机制。新兴的转基因和干细胞技术在不久的将来也应该能提供一个非常有价值的兔实验模型。
