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Novel MYH11 and ACTA2 mutations reveal a role for enhanced TGFβ signaling in FTAAD.新发现的 MYH11 和 ACTA2 突变表明 TGFβ 信号通路的增强在 FTAAD 中起作用。
Int J Cardiol. 2013 May 10;165(2):314-21. doi: 10.1016/j.ijcard.2011.08.079. Epub 2011 Sep 19.
2
Exome sequencing identifies SMAD3 mutations as a cause of familial thoracic aortic aneurysm and dissection with intracranial and other arterial aneurysms.外显子组测序鉴定出 SMAD3 突变是家族性胸主动脉瘤和夹层伴颅内及其他动脉动脉瘤的病因。
Circ Res. 2011 Sep 2;109(6):680-6. doi: 10.1161/CIRCRESAHA.111.248161. Epub 2011 Jul 21.
3
Mutations in SMAD3 cause a syndromic form of aortic aneurysms and dissections with early-onset osteoarthritis.SMAD3 基因突变可导致综合征型主动脉瘤和夹层，伴发病症有早发性骨关节炎。
Nat Genet. 2011 Feb;43(2):121-6. doi: 10.1038/ng.744. Epub 2011 Jan 9.
4
Isolated thoracic aortitis: clinicopathological and immunohistochemical study of 11 cases.孤立性胸主动脉炎：11 例临床病理和免疫组化研究。
Cardiovasc Pathol. 2011 Nov-Dec;20(6):352-60. doi: 10.1016/j.carpath.2010.09.003. Epub 2010 Oct 30.
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The Gulstonian Lectures, on Malignant Endocarditis.关于恶性心内膜炎的古尔斯顿讲座
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A continuous observation of the degenerative process in the intervertebral disc of Smad3 gene knock-out mice.对Smad3基因敲除小鼠椎间盘退变过程的持续观察。
Spine (Phila Pa 1976). 2009 Jun 1;34(13):1363-9. doi: 10.1097/BRS.0b013e3181a3c7c7.
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A new clinicopathological entity of IgG4-related inflammatory abdominal aortic aneurysm.IgG4相关性炎性腹主动脉瘤的一种新的临床病理实体。
J Vasc Surg. 2009 May;49(5):1264-71; discussion 1271. doi: 10.1016/j.jvs.2008.11.072. Epub 2009 Feb 14.
8
Histopathologic findings in ascending aortas from individuals with Loeys-Dietz syndrome (LDS).洛伊斯-迪茨综合征（LDS）患者升主动脉的组织病理学发现。
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9
Angiotensin II blockade and aortic-root dilation in Marfan's syndrome.马凡综合征中的血管紧张素 II 阻断与主动脉根部扩张
N Engl J Med. 2008 Jun 26;358(26):2787-95. doi: 10.1056/NEJMoa0706585.
10
Mutations in smooth muscle alpha-actin (ACTA2) lead to thoracic aortic aneurysms and dissections.平滑肌α-肌动蛋白（ACTA2）突变会导致胸主动脉瘤和主动脉夹层。
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主动脉瘤：病因发病机制与临床病理相关性

Aortic Aneurysm: Etiopathogenesis and Clinicopathologic Correlations.

作者信息

Ikeda Yoshihiko

机构信息

Department of Pathology, National Cerebral and Cardiovascular Center, Suita, Osaka, Japan.

出版信息

Ann Vasc Dis. 2016;9(2):73-9. doi: 10.3400/avd.ra.16-00018. Epub 2016 Apr 7.

DOI:10.3400/avd.ra.16-00018
PMID:27375798
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4919297/
Abstract

Aortic aneurysm (AA) is one of the life-threatening aortic diseases, leading to aortic rupture of any cause including atherosclerotic and non-atherosclerotic diseases. AA is diagnosed in a variable proportion of patients with dilated aorta by imaging modality. The etiopathogenesis of AA remains unclear in many aortic diseases. Furthermore, although it may be difficult to explain all phenotypes of patients even if genetic mutation could be identified in some proteins such as smooth muscle cell α-actin (ACTA2), myosin heavy chain 11 (MYH11) or SMAD3, individualized consideration of these factors in each patient is essential on the basis of clinicopathological characteristics.

摘要

主动脉瘤（AA）是一种危及生命的主动脉疾病，可导致因任何原因引起的主动脉破裂，包括动脉粥样硬化性和非动脉粥样硬化性疾病。通过影像学检查，在不同比例的主动脉扩张患者中可诊断出AA。在许多主动脉疾病中，AA的病因发病机制仍不清楚。此外，尽管即使在某些蛋白质如平滑肌细胞α-肌动蛋白（ACTA2）、肌球蛋白重链11（MYH11）或SMAD3中发现基因突变，也可能难以解释所有患者的表型，但根据临床病理特征对每个患者的这些因素进行个体化考虑至关重要。