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用于研究CA形成潜在机制的实验动物模型的开发与应用。

The development and the use of experimental animal models to study the underlying mechanisms of CA formation.

作者信息

Aoki Tomohiro, Nishimura Masaki

机构信息

Department of Neurosurgery, Graduate School of Medicine, Kyoto University, 54 Kawaharacho, Shogoin, Sakyo-ku, Kyoto 606-8501, Japan.

出版信息

J Biomed Biotechnol. 2011;2011:535921. doi: 10.1155/2011/535921. Epub 2010 Dec 28.

DOI:10.1155/2011/535921
PMID:21253583
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3018658/
Abstract

Cerebral aneurysms (CAs) have a high prevalence and can cause a lethal subarachnoid hemorrhage. Currently, CAs can only be treated with invasive surgical procedures. To unravel the underlying mechanisms of CA formation and to develop new therapeutic drugs for CAs, animal models of CA have been established, modified, and analyzed. Experimental findings from these models have clarified some of the potential mechanisms of CA formation, especially the relationship between hemodynamic stress and chronic inflammation. Increased hemodynamic stress acting at the site of bifurcation of cerebral arteries triggers an inflammatory response mediated by various proinflammatory molecules in arterial walls, inducing pathological changes in the models similar to those observed in the walls of human CAs. Findings from animal studies have provided new insights into CA formation and may contribute to the development of new therapeutic drugs for CAs.

摘要

脑动脉瘤(CAs)患病率高,可导致致命的蛛网膜下腔出血。目前,脑动脉瘤只能通过侵入性外科手术治疗。为了阐明脑动脉瘤形成的潜在机制并开发针对脑动脉瘤的新型治疗药物,人们建立、改进并分析了脑动脉瘤动物模型。这些模型的实验结果阐明了脑动脉瘤形成的一些潜在机制,尤其是血流动力学应激与慢性炎症之间的关系。作用于脑动脉分叉部位的血流动力学应激增加会触发由动脉壁中各种促炎分子介导的炎症反应,在模型中诱导出与人类脑动脉瘤壁中观察到的病理变化相似的变化。动物研究结果为脑动脉瘤的形成提供了新的见解,并可能有助于开发针对脑动脉瘤的新型治疗药物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/23a7/3018658/55d76fa8c8ba/JBB2011-535921.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/23a7/3018658/7f8bcd2788bb/JBB2011-535921.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/23a7/3018658/9c099953a52d/JBB2011-535921.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/23a7/3018658/55d76fa8c8ba/JBB2011-535921.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/23a7/3018658/7f8bcd2788bb/JBB2011-535921.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/23a7/3018658/9c099953a52d/JBB2011-535921.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/23a7/3018658/55d76fa8c8ba/JBB2011-535921.003.jpg

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Curr Neurovasc Res. 2010 May;7(2):113-24. doi: 10.2174/156720210791184916.
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Targeting chronic inflammation in cerebral aneurysms: focusing on NF-kappaB as a putative target of medical therapy.
Cardiovasc Res. 2025 Jun 12;121(6):915-928. doi: 10.1093/cvr/cvaf063.
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