摘要
背景:腹主动脉瘤(Aaa)影响约10%的大于或等于65岁患者,常与高血压、血脂异常及其他与生活方式有关的疾病有关。腹主动脉瘤的发生与动脉硬化性改变伴发慢性炎症有关。然而,与动脉粥样硬化相关的确切病理机制仍不确定,为什么只有特定人群/百分比的动脉硬化患者发生动脉瘤,以及糖尿病如何抑制动脉瘤的发展仍未得到解答。 目的:通过对人AAA组织的病理组织学分析,探讨一种新的AAA形成机制,并在此基础上建立与人AAA组织相似的AAA动物模型。 结果:最近我们发现主动脉节段血管狭窄表现为扩张,主动脉是我们循环系统中最大的动脉,在生理条件下,主动脉内层是通过从腔内血流中直接扩散营养物质来营养的,而外膜主要由静脉灌注,因此大血管壁内的小营养动脉及静脉的低灌注会导致缺氧和随后的炎症和主动脉壁组织变性,从而导致动脉瘤的形成。在此基础上,我们通过降低大血管壁内的小营养动脉及静脉到主动脉壁的血流量,建立了AAA动物模型,成功地复制了AAA动物模型,该模型与人的组织病理学观察结果不一致,并观察到血管外膜脂质成分的明显异常。 结论:主动脉壁低灌注可引起炎症性AAA,为治疗AAA提供了新的治疗靶点。
关键词: 低灌注,血管外膜,腹主动脉瘤,炎症,组织变性,新疗法。
图形摘要
Current Drug Targets
Title:Hypoperfusion of the Aortic Wall Secondary to Degeneration of Adventitial Vasa Vasorum Causes Abdominal Aortic Aneurysms
Volume: 19 Issue: 11
关键词: 低灌注,血管外膜,腹主动脉瘤,炎症,组织变性,新疗法。
摘要: Background: An abdominal aortic aneurysm (AAA), which affects approximately 10% of Japanese men aged ≥ 65 years, is frequently associated with hypertension, dyslipidemia, and other lifestyle- related diseases. The development of an AAA is attributed to chronic inflammation concomitant with arteriosclerotic changes. However, an accurate pathomechanism associated with AAA remains uncertain, and questions such as why only a particular group/percentage of patients with arteriosclerosis develop aneurysms and how diabetes suppresses aneurysm development remain unanswered.
Objective: We examined a novel mechanism to develop AAA based on histopathological findings following analysis of the human AAA tissues. Additionally, based on these findings, we developed a new animal model of AAA, in which the histopathological characteristics are similar to human AAA tissue.
Results: Recently, we identified stenosis of the vasa vasorum (VV) in aortic segments showing dilatation. The aorta is the largest artery in our circulatory system. Under physiological conditions, the inner layer of the aorta is nourished via direct diffusion of nutrients from the luminal blood flow, whereas the outer adventitia is primarily perfused by the VV. Therefore, hypoperfusion of the VV induces hypoxia and subsequent inflammation and tissue degeneration of the aortic wall, resulting in aneurysm formation.
Based on these findings, we established an AAA animal model by reducing the blood flow through the VV to the aortic wall. AAA was successfully reproduced in our animal model. Histopathological findings in this model were indistinguishable from those observed in humans, and pronounced abnormality in lipid composition in blood vessel adventitia was also observed.
Conclusion: Thus, hypoperfusion of the aortic wall appeared to be sufficient to cause inflammationinduced AAA. These findings may provide potential targets for novel therapeutics for the management of an AAA.
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Cite this article as:
Hypoperfusion of the Aortic Wall Secondary to Degeneration of Adventitial Vasa Vasorum Causes Abdominal Aortic Aneurysms, Current Drug Targets 2018; 19 (11) . https://dx.doi.org/10.2174/1389450119666180122154409
DOI https://dx.doi.org/10.2174/1389450119666180122154409 |
Print ISSN 1389-4501 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5592 |
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