SR-BI and ApoE knockout animals and use thereof as models for atherosclerosis and heart attack
    2.
    发明授权
    SR-BI and ApoE knockout animals and use thereof as models for atherosclerosis and heart attack 失效
    SR-BI和ApoE敲除动物,并将其用作动脉粥样硬化和心脏病发作的模型

    公开(公告)号:US06437215B1

    公开(公告)日:2002-08-20

    申请号:US09606324

    申请日:2000-06-28

    IPC分类号: A01K67027

    摘要: Transgenic animals that do not express functional SR-BI and ApoE develop severe atherosclerosis, by age four weeks in transgenic mice. Moreover, these animals exhibit progressive heart block by age four weeks, and die by age nine weeks. Pathology shows extensive fibrosis of the heart and occlusion of coronary arteries. The occlusion appears to be due to clotting, since fat deposition is in the walls. These animals are good models for the following diseases, and for screening of drugs useful in the treatment and/or prevention of these disorders: cardiac fibrosis, myocardial infarction, defects in electrical conductance, atherosclerosis, unstable plaque, and stroke. In contrast to other known models for atherosclerosis, these animals do not have to be fed extreme diets for long periods before developing atherosclerosis. No other known model for heart attacks and stroke is known.

    摘要翻译: 不表达功能性SR-BI和ApoE的转基因动物在转基因小鼠中4周龄时出现严重的动脉粥样硬化。 此外,这些动物在四周时间内呈现进行性心脏阻塞,并且死亡9周。 病理显示广泛的心脏纤维化和冠状动脉闭塞。 闭塞似乎是由于凝血,因为脂肪沉积在墙壁中。 这些动物是以下疾病的良好模型,并且用于筛选用于治疗和/或预防这些疾病的药物:心脏纤维化,心肌梗塞,电导缺陷,动脉粥样硬化,不稳定斑块和中风。 与其他已知的动脉粥样硬化模型相反,这些动物在发展动脉粥样硬化之前不必长时间喂食极限饮食。 没有其他已知的心脏病发作和中风模型已知。