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本文引用的文献

1
Prolonged infusion of angiotensin II in apoE(-/-) mice promotes macrophage recruitment with continued expansion of abdominal aortic aneurysm.在载脂蛋白 E 基因敲除(apoE(-/-))小鼠中持续输注血管紧张素 II 可促进巨噬细胞募集,并持续扩大腹主动脉瘤。
Am J Pathol. 2011 Sep;179(3):1542-8. doi: 10.1016/j.ajpath.2011.05.049. Epub 2011 Jul 19.
2
Statins exert differential effects on angiotensin II-induced atherosclerosis, but no benefit for abdominal aortic aneurysms.他汀类药物对血管紧张素 II 诱导的动脉粥样硬化有不同的作用,但对腹主动脉瘤没有益处。
Atherosclerosis. 2011 Jul;217(1):90-6. doi: 10.1016/j.atherosclerosis.2011.03.005. Epub 2011 Mar 10.
3
TGF-beta activity protects against inflammatory aortic aneurysm progression and complications in angiotensin II-infused mice.TGF-β 活性可防止血管紧张素 II 输注小鼠的炎症性主动脉瘤进展和并发症。
J Clin Invest. 2010 Feb;120(2):422-32. doi: 10.1172/JCI38136. Epub 2010 Jan 25.
4
An adventitial IL-6/MCP1 amplification loop accelerates macrophage-mediated vascular inflammation leading to aortic dissection in mice.血管外膜 IL-6/MCP1 扩增环加速巨噬细胞介导的血管炎症反应,导致小鼠主动脉夹层。
J Clin Invest. 2009 Dec;119(12):3637-51. doi: 10.1172/JCI38308. Epub 2009 Nov 16.
5
Obesity promotes inflammation in periaortic adipose tissue and angiotensin II-induced abdominal aortic aneurysm formation.肥胖会促进主动脉周围脂肪组织的炎症反应以及血管紧张素II诱导的腹主动脉瘤形成。
Arterioscler Thromb Vasc Biol. 2009 Oct;29(10):1458-64. doi: 10.1161/ATVBAHA.109.192658. Epub 2009 Jul 16.
6
The role of the renin-angiotensin system in aortic aneurysmal diseases.肾素-血管紧张素系统在主动脉瘤疾病中的作用。
Curr Hypertens Rep. 2008 Apr;10(2):99-106. doi: 10.1007/s11906-008-0020-3.
7
Medical management of small abdominal aortic aneurysms.小腹部主动脉瘤的医学管理。
Circulation. 2008 Apr 8;117(14):1883-9. doi: 10.1161/CIRCULATIONAHA.107.735274.
8
Angiotensin II type 1 receptor 1166C polymorphism is associated with abdominal aortic aneurysm in three independent cohorts.血管紧张素II 1型受体1166C多态性在三个独立队列中与腹主动脉瘤相关。
Arterioscler Thromb Vasc Biol. 2008 Apr;28(4):764-70. doi: 10.1161/ATVBAHA.107.155564. Epub 2008 Jan 31.
9
Inhibited aortic aneurysm formation in BLT1-deficient mice.BLT1基因缺陷小鼠的主动脉瘤形成受到抑制。
J Immunol. 2007 Jul 1;179(1):691-7. doi: 10.4049/jimmunol.179.1.691.
10
Angiotensin-converting enzyme inhibitors and aortic rupture: a population-based case-control study.血管紧张素转换酶抑制剂与主动脉破裂:一项基于人群的病例对照研究。
Lancet. 2006 Aug 19;368(9536):659-65. doi: 10.1016/S0140-6736(06)69250-7.

血管紧张素 II 诱导的腹主动脉瘤的复杂病理。

Complex pathologies of angiotensin II-induced abdominal aortic aneurysms.

机构信息

Saha Cardiovascular Research Center, University of Kentucky, Lexington, KY 40536-0509, USA.

出版信息

J Zhejiang Univ Sci B. 2011 Aug;12(8):624-8. doi: 10.1631/jzus.B1101002.

DOI:10.1631/jzus.B1101002
PMID:21796801
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3150714/
Abstract

Angiotensin II (AngII) is the primary bioactive peptide of the renin angiotensin system that plays a critical role in many cardiovascular diseases. Subcutaneous infusion of AngII into mice induces the development of abdominal aortic aneurysms (AAAs). Like human AAAs, AngII-induced AAA tissues exhibit progressive changes and considerable heterogeneity. This complex pathology provides an impediment to the quantification of aneurysmal tissue composition by biochemical and immunostaining techniques. Therefore, while the mouse model of AngII-induced AAAs provides a salutary approach to studying the mechanisms of the evolution of AAAs in humans, meaningful interpretation of mechanisms requires consideration of the heterogeneous nature of the diseased tissue.

摘要

血管紧张素 II(AngII)是肾素-血管紧张素系统的主要生物活性肽,在许多心血管疾病中发挥着关键作用。将 AngII 皮下输注到小鼠体内会诱导腹主动脉瘤(AAA)的发展。与人类的 AAA 一样,AngII 诱导的 AAA 组织表现出进行性变化和相当大的异质性。这种复杂的病理学为通过生化和免疫染色技术定量动脉瘤组织成分带来了阻碍。因此,虽然 AngII 诱导的 AAA 小鼠模型为研究人类 AAA 演变的机制提供了有益的方法,但要对机制进行有意义的解释,就需要考虑病变组织的异质性。