Bond Andrew R, Jackson Christopher L
Bristol Heart Institute, University of Bristol, Bristol Royal Infirmary, Bristol, UK.
J Biomed Biotechnol. 2011;2011:379069. doi: 10.1155/2011/379069. Epub 2010 Nov 7.
Atherosclerosis has been studied in animals for almost a century, yet the events leading up to the rupture of an atherosclerotic plaque (the underlying cause of the majority of fatal thrombosis formation) have only been studied in the past decade, due in part to the development of a mouse model of spontaneous plaque rupture. Apolipoprotein E knockout mice, when fed a high-fat diet, consistently develop lesions in the brachiocephalic artery that rupture at a known time point. It is therefore now possible to observe the development of lesions to elucidate the mechanisms behind the rupture of plaques. Critics argue that the model does not replicate the appearance of human atherosclerotic plaque ruptures. The purpose of this review is to highlight the reasons why we should be looking to the apolipoprotein E knockout mouse to further our understanding of plaque rupture.
动脉粥样硬化在动物身上的研究已近一个世纪，但直至过去十年，才开始对导致动脉粥样硬化斑块破裂（多数致命血栓形成的根本原因）的相关事件展开研究，部分原因是自发斑块破裂小鼠模型的出现。载脂蛋白E基因敲除小鼠在喂食高脂饮食后，会在头臂动脉持续形成病变，并在已知时间点破裂。因此，现在有可能观察病变的发展过程，以阐明斑块破裂背后的机制。批评者认为，该模型无法复制人类动脉粥样硬化斑块破裂的表现。本综述的目的是强调我们为何应借助载脂蛋白E基因敲除小鼠来加深对斑块破裂的理解。
