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本文引用的文献

1
TNF induction of jagged-1 in endothelial cells is NFkappaB-dependent.肿瘤坏死因子诱导内皮细胞中锯齿蛋白-1的表达是依赖核因子κB的。
Gene. 2009 Apr 15;435(1-2):36-44. doi: 10.1016/j.gene.2009.01.003. Epub 2009 Jan 22.
2
Angiogenesis: a team effort coordinated by notch.血管生成:由Notch协调的团队协作。
Dev Cell. 2009 Feb;16(2):196-208. doi: 10.1016/j.devcel.2009.01.015.
3
Endothelial-mural cell signaling in vascular development and angiogenesis.血管发育和血管生成中的内皮细胞-壁细胞信号传导
Arterioscler Thromb Vasc Biol. 2009 May;29(5):630-8. doi: 10.1161/ATVBAHA.107.161521. Epub 2009 Jan 22.
4
Critical role of tissue kallikrein in vessel formation and maturation: implications for therapeutic revascularization.组织激肽释放酶在血管形成和成熟中的关键作用:对治疗性血管再生的意义。
Arterioscler Thromb Vasc Biol. 2009 May;29(5):657-64. doi: 10.1161/ATVBAHA.108.182139. Epub 2009 Jan 22.
5
Nrarp coordinates endothelial Notch and Wnt signaling to control vessel density in angiogenesis.Nrarp协调内皮细胞中的Notch和Wnt信号传导,以控制血管生成中的血管密度。
Dev Cell. 2009 Jan;16(1):70-82. doi: 10.1016/j.devcel.2008.12.009.
6
NOTCH3 expression is induced in mural cells through an autoregulatory loop that requires endothelial-expressed JAGGED1.NOTCH3表达通过一个需要内皮细胞表达的JAGGED1的自调节环在壁细胞中被诱导。
Circ Res. 2009 Feb 27;104(4):466-75. doi: 10.1161/CIRCRESAHA.108.184846. Epub 2009 Jan 15.
7
DLL1-mediated Notch activation regulates endothelial identity in mouse fetal arteries.DLL1介导的Notch激活调节小鼠胎儿动脉中的内皮细胞特性。
Blood. 2009 May 28;113(22):5680-8. doi: 10.1182/blood-2008-08-174508. Epub 2009 Jan 14.
8
Loss of Notch signalling induced by Dll4 causes arterial calibre reduction by increasing endothelial cell response to angiogenic stimuli.由Dll4诱导的Notch信号缺失通过增强内皮细胞对血管生成刺激的反应导致动脉管径减小。
BMC Dev Biol. 2008 Dec 16;8:117. doi: 10.1186/1471-213X-8-117.
9
Notch1 is an effector of Akt and hypoxia in melanoma development.Notch1是Akt和缺氧在黑色素瘤发展过程中的效应分子。
J Clin Invest. 2008 Nov;118(11):3660-70. doi: 10.1172/JCI36157. Epub 2008 Oct 16.
10
Critical limb ischemia: medical and surgical management.严重肢体缺血:内科与外科治疗
Vasc Med. 2008 Aug;13(3):281-91. doi: 10.1177/1358863X08091485.

Notch 信号通路在缺血诱导的血管生成中的作用。

Notch signalling in ischaemia-induced angiogenesis.

机构信息

Experimental Cardiovascular Medicine, Bristol Heart Institute, University of Bristol, Bristol, UK.

出版信息

Biochem Soc Trans. 2009 Dec;37(Pt 6):1221-7. doi: 10.1042/BST0371221.

DOI:10.1042/BST0371221
PMID:19909251
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2821013/
Abstract

Notch signalling represents a key pathway essential for normal vascular development. Recently, great attention has been focused on the implication of Notch pathway components in postnatal angiogenesis and regenerative medicine. This paper critically reviews the most recent findings supporting the role of Notch in ischaemia-induced neovascularization. Notch signalling reportedly regulates several steps of the reparative process occurring in ischaemic tissues, including sprouting angiogenesis, vessel maturation, interaction of vascular cells with recruited leucocytes and skeletal myocyte regeneration. Further characterization of Notch interaction with other signalling pathways might help identify novel targets for therapeutic angiogenesis.

摘要

Notch 信号通路是正常血管发育所必需的关键途径。最近,人们越来越关注 Notch 通路成分在血管生成和再生医学中的作用。本文批判性地回顾了支持 Notch 在缺血诱导的新生血管形成中的作用的最新发现。据报道,Notch 信号通路调节缺血组织中发生的修复过程的几个步骤,包括发芽血管生成、血管成熟、血管细胞与募集的白细胞的相互作用以及骨骼肌细胞的再生。进一步研究 Notch 与其他信号通路的相互作用可能有助于确定治疗性血管生成的新靶点。