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SR-B1基因敲除/ApoE基因R61h纯合突变小鼠可模拟人类冠心病。

SR-B1-/-ApoE-R61h/h Mice Mimic Human Coronary Heart Disease.

作者信息

Staršíchová Andrea

机构信息

Graduate School Cell Dynamics and Disease, University of Muenster, Muenster, Germany.

European Institute for Molecular Imaging, University of Muenster, Muenster, Germany.

出版信息

Cardiovasc Drugs Ther. 2024 Dec;38(6):1123-1137. doi: 10.1007/s10557-023-07475-8. Epub 2023 Jun 5.

Abstract

Cardiovascular diseases are the leading cause of death in the modern world. Atherosclerosis underlies the majority of these pathologies and may result in sudden life-threatening events such as myocardial infarction or stroke. Current concepts consider a rupture (resp. erosion) of "unstable/vulnerable" atherosclerotic plaques as a primary cause leading to thrombus formation and subsequent occlusion of the artery lumen finally triggering an acute clinical event. We and others described SR-B1-/-ApoE-R61h/h mice mimicking clinical coronary heart disease in all major aspects: from coronary atherosclerosis through vulnerable plaque ruptures leading to thrombus formation/coronary artery occlusion, finally resulting in myocardial infarction/ischemia. SR-B1-/-ApoE-R61h/h mouse provides a valuable model to study vulnerable/occlusive plaques, to evaluate bioactive compounds as well as new anti-inflammatory and "anti-rupture" drugs, and to test new technologies in experimental cardiovascular medicine. This review summarizes and discuss our knowledge about SR-B1-/-ApoE-R61h/h mouse model based on recent publications and experimental observations from the lab.

摘要

心血管疾病是现代世界的主要死因。动脉粥样硬化是这些病理状况的主要原因,可能导致心肌梗死或中风等危及生命的突发情况。目前的观点认为,“不稳定/易损”动脉粥样硬化斑块的破裂(或糜烂)是导致血栓形成以及随后动脉管腔闭塞并最终引发急性临床事件的主要原因。我们和其他人描述了SR-B1-/-ApoE-R61h/h小鼠,该小鼠在所有主要方面模拟临床冠心病:从冠状动脉粥样硬化到易损斑块破裂导致血栓形成/冠状动脉闭塞,最终导致心肌梗死/缺血。SR-B1-/-ApoE-R61h/h小鼠为研究易损/闭塞性斑块、评估生物活性化合物以及新型抗炎和“抗破裂”药物,以及在实验性心血管医学中测试新技术提供了一个有价值的模型。本综述基于最近的出版物和实验室的实验观察结果,总结并讨论了我们对SR-B1-/-ApoE-R61h/h小鼠模型的认识。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f181/10240136/ec6651440c2d/10557_2023_7475_Fig1_HTML.jpg

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