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动脉壁的发育和病理学。

Development and pathologies of the arterial wall.

机构信息

Section of Cardiovascular Medicine, Department of Internal Medicine, Yale Cardiovascular Research Center, Yale University School of Medicine, 300 George St., Rm 773J, New Haven, CT, 06511, USA.

出版信息

Cell Mol Life Sci. 2014 Jun;71(11):1977-99. doi: 10.1007/s00018-013-1478-y. Epub 2013 Sep 27.

DOI:10.1007/s00018-013-1478-y
PMID:24071897
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11113178/
Abstract

Arteries consist of an inner single layer of endothelial cells surrounded by layers of smooth muscle and an outer adventitia. The majority of vascular developmental studies focus on the construction of endothelial networks through the process of angiogenesis. Although many devastating vascular diseases involve abnormalities in components of the smooth muscle and adventitia (i.e., the vascular wall), the morphogenesis of these layers has received relatively less attention. Here, we briefly review key elements underlying endothelial layer formation and then focus on vascular wall development, specifically on smooth muscle cell origins and differentiation, patterning of the vascular wall, and the role of extracellular matrix and adventitial progenitor cells. Finally, we discuss select human diseases characterized by marked vascular wall abnormalities. We propose that continuing to apply approaches from developmental biology to the study of vascular disease will stimulate important advancements in elucidating disease mechanism and devising novel therapeutic strategies.

摘要

动脉由一层内层的内皮细胞组成,周围是多层平滑肌和外层的外膜。大多数血管发育研究都集中在通过血管生成过程构建内皮网络上。尽管许多严重的血管疾病涉及平滑肌和外膜(即血管壁)成分的异常,但这些层的形态发生受到的关注相对较少。在这里,我们简要回顾内皮层形成的关键要素,然后重点讨论血管壁的发育,特别是平滑肌细胞的起源和分化、血管壁的模式形成以及细胞外基质和外膜祖细胞的作用。最后,我们讨论了一些以明显的血管壁异常为特征的人类疾病。我们认为,继续将发育生物学的方法应用于血管疾病的研究将刺激在阐明疾病机制和设计新的治疗策略方面的重要进展。

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本文引用的文献

1
An endothelial apelin-FGF link mediated by miR-424 and miR-503 is disrupted in pulmonary arterial hypertension.内皮细胞中由 miR-424 和 miR-503 介导的 Apelin-FGF 联系在肺动脉高压中被破坏。
Nat Med. 2013 Jan;19(1):74-82. doi: 10.1038/nm.3040. Epub 2012 Dec 23.
2
FGF regulates TGF-β signaling and endothelial-to-mesenchymal transition via control of let-7 miRNA expression.FGF 通过调控 let-7 miRNA 的表达来调节 TGF-β 信号和血管内皮细胞向间充质细胞的转化。
Cell Rep. 2012 Dec 27;2(6):1684-96. doi: 10.1016/j.celrep.2012.10.021. Epub 2012 Nov 29.
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VEGF and Notch in tip and stalk cell selection.血管内皮生长因子(VEGF)和 Notch 在顶端和茎细胞选择中的作用。
Cold Spring Harb Perspect Med. 2013 Jan 1;3(1):a006569. doi: 10.1101/cshperspect.a006569.
4
The sphingosine-1-phosphate receptor S1PR1 restricts sprouting angiogenesis by regulating the interplay between VE-cadherin and VEGFR2.鞘氨醇-1-磷酸受体 S1PR1 通过调节 VE-钙黏蛋白和 VEGFR2 之间的相互作用来限制血管生成。
Dev Cell. 2012 Sep 11;23(3):587-99. doi: 10.1016/j.devcel.2012.08.005.
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Radial construction of an arterial wall.动脉壁的径向构建。
Dev Cell. 2012 Sep 11;23(3):482-93. doi: 10.1016/j.devcel.2012.07.009.
6
S1P1 inhibits sprouting angiogenesis during vascular development.S1P1 抑制血管发育过程中的血管生成。
Development. 2012 Oct;139(20):3859-69. doi: 10.1242/dev.078550. Epub 2012 Sep 5.
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Structure and function of the mammalian fibrillin gene family: implications for human connective tissue diseases.哺乳动物原纤维蛋白基因家族的结构与功能:对人类结缔组织疾病的影响。
Mol Genet Metab. 2012 Dec;107(4):635-47. doi: 10.1016/j.ymgme.2012.07.023. Epub 2012 Aug 3.
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Determination of endothelial stalk versus tip cell potential during angiogenesis by H2.0-like homeobox-1.通过 H2.0 样同源盒-1 确定血管生成过程中内皮干/尖端细胞潜能。
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