Extracellular matrix, regional heterogeneity of the aorta, and aortic aneurysm.,Experimental & Molecular Medicine

当前位置： X-MOL 学术 › Exp. Mol. Med. › 论文详情

Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)

Extracellular matrix, regional heterogeneity of the aorta, and aortic aneurysm.
Experimental & Molecular Medicine ( IF 9.5 ) Pub Date : 2019-12-19 , DOI: 10.1038/s12276-019-0286-3
Sayantan Jana ₁ , Mei Hu ₁ , Mengcheng Shen ₂ , Zamaneh Kassiri ₁

Affiliation

Aortic aneurysm is an asymptomatic disease with dire outcomes if undiagnosed. Aortic aneurysm rupture is a significant cause of death worldwide. To date, surgical repair or endovascular repair (EVAR) is the only effective treatment for aortic aneurysm, as no pharmacological treatment has been found effective. Aortic aneurysm, a focal dilation of the aorta, can be formed in the thoracic (TAA) or the abdominal (AAA) region; however, our understanding as to what determines the site of aneurysm formation remains quite limited. The extracellular matrix (ECM) is the noncellular component of the aortic wall, that in addition to providing structural support, regulates bioavailability of an array of growth factors and cytokines, thereby influencing cell function and behavior that ultimately determine physiological or pathological remodeling of the aortic wall. Here, we provide an overview of the ECM proteins that have been reported to be involved in aortic aneurysm formation in humans or animal models, and the experimental models for TAA and AAA and the link to ECM manipulations. We also provide a comparative analysis, where data available, between TAA and AAA, and how aberrant ECM proteolysis versus disrupted synthesis may determine the site of aneurysm formation.

中文翻译：

细胞外基质、主动脉的区域异质性和主动脉瘤。

主动脉瘤是一种无症状疾病，如果未确诊，后果会很严重。主动脉瘤破裂是全世界死亡的重要原因。迄今为止，手术修复或血管内修复 (EVAR) 是主动脉瘤唯一有效的治疗方法，因为尚未发现药物治疗有效。主动脉瘤是主动脉的局灶性扩张，可以在胸腔 (TAA) 或腹部 (AAA) 区域形成；然而，我们对决定动脉瘤形成部位的因素的理解仍然非常有限。细胞外基质 (ECM) 是主动脉壁的非细胞成分，除了提供结构支持外，还调节一系列生长因子和细胞因子的生物利用度，从而影响最终决定主动脉壁生理或病理重塑的细胞功能和行为。在这里，我们概述了据报道在人类或动物模型中参与主动脉瘤形成的 ECM 蛋白，以及 TAA 和 AAA 的实验模型以及与 ECM 操作的联系。我们还提供了 TAA 和 AAA 之间可用数据的比较分析，以及异常 ECM 蛋白水解与中断合成如何确定动脉瘤形成的部位。

更新日期：2019-12-19

点击分享查看原文

点击收藏

公开下载

阅读更多本刊最新论文