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细胞骨架在血管生成芽的形成和维持中的作用。

Role of the cytoskeleton in formation and maintenance of angiogenic sprouts.

作者信息

Bayless Kayla J, Johnson Greg A

机构信息

Department of Molecular and Cellular Medicine, Texas A&M Health Science Center, College Station, TX 77843-1114, USA.

出版信息

J Vasc Res. 2011;48(5):369-85. doi: 10.1159/000324751. Epub 2011 Apr 4.

DOI:10.1159/000324751
PMID:21464572
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3080587/
Abstract

Angiogenesis is the formation of new blood vessels from pre-existing structures, and is a key step in tissue and organ development, wound healing and pathological events. Changes in cell shape orchestrated by the cytoskeleton are integral to accomplishing the various steps of angiogenesis, and an intact cytoskeleton is also critical for maintaining newly formed structures. This review focuses on how the 3 main cytoskeletal elements--microfilaments, microtubules, and intermediate filaments--regulate the formation and maintenance of angiogenic sprouts. Multiple classes of compounds target microtubules and microfilaments, revealing much about the role of actin and tubulin and their associated molecules in angiogenic sprout formation and maintenance. In contrast, intermediate filaments are much less studied, yet intriguing evidence suggests a vital, but unresolved, role in angiogenic sprouting. This review discusses evidence for regulatory molecules and pharmacological compounds that affect actin, microtubule and intermediate filament dynamics to alter various steps of angiogenesis, including endothelial sprout formation and maintenance.

摘要

血管生成是指从已有的结构中形成新的血管,是组织和器官发育、伤口愈合及病理过程中的关键步骤。由细胞骨架精心编排的细胞形状变化是完成血管生成各个步骤所不可或缺的,完整的细胞骨架对于维持新形成的结构也至关重要。本综述聚焦于3种主要的细胞骨架成分——微丝、微管和中间丝——如何调节血管生成芽的形成和维持。多类化合物作用于微管和微丝,这揭示了肌动蛋白、微管蛋白及其相关分子在血管生成芽形成和维持中的作用。相比之下,对中间丝的研究要少得多,但有趣的证据表明其在血管生成芽形成中起着至关重要但尚未明确的作用。本综述讨论了影响肌动蛋白、微管和中间丝动力学以改变血管生成各个步骤(包括内皮芽的形成和维持)的调节分子和药理化合物的相关证据。

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Cdc42-mediated inhibition of GSK-3β improves angio-architecture and lumen formation during VEGF-driven pathological angiogenesis.Cdc42 介导的 GSK-3β 抑制作用可改善 VEGF 驱动的病理性血管生成过程中的血管生成结构和管腔形成。
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