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细胞外基质在生理和病理条件下调节血管生成。

Extracellular matrix modulates angiogenesis in physiological and pathological conditions.

作者信息

Neve Anna, Cantatore Francesco Paolo, Maruotti Nicola, Corrado Addolorata, Ribatti Domenico

机构信息

Rheumatology Clinic, Department of Medical and Surgical Sciences, University of Foggia, Ospedale "Col. D'Avanzo", 71121 Foggia, Italy.

Department of Basic Medical Sciences, Neurosciences and Sensory Organs, Section of Human Anatomy and Histology, University of Bari Medical School, 70124 Bari, Italy ; National Cancer Institute "Giovanni Paolo", 70124 Bari, Italy.

出版信息

Biomed Res Int. 2014;2014:756078. doi: 10.1155/2014/756078. Epub 2014 May 18.

DOI:10.1155/2014/756078
PMID:24949467
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4052469/
Abstract

Angiogenesis is a multistep process driven by a wide range of positive and negative regulatory factors. Extracellular matrix (ECM) plays a crucial role in the regulation of this process. The degradation of ECM, occurring in response to an angiogenic stimulus, leads to degradation or partial modification of matrix molecules, release of soluble factors, and exposure of cryptic sites with pro- and/or antiangiogenic activity. ECM molecules and fragments, resulting from proteolysis, can also act directly as inflammatory stimuli, and this can explain the exacerbated angiogenesis that drives and maintains several inflammatory diseases. In this review we have summarized some of the more recent literature data concerning the molecular control of ECM in angiogenesis in both physiological and pathological conditions.

摘要

血管生成是一个由多种正负调节因子驱动的多步骤过程。细胞外基质(ECM)在这一过程的调节中起着关键作用。ECM的降解是对血管生成刺激的反应,导致基质分子的降解或部分修饰、可溶性因子的释放以及具有促血管生成和/或抗血管生成活性的隐蔽位点的暴露。蛋白水解产生的ECM分子和片段也可直接作为炎症刺激物,这可以解释驱动和维持几种炎症性疾病的血管生成加剧现象。在这篇综述中,我们总结了一些关于生理和病理条件下血管生成中ECM分子控制的最新文献数据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c1c/4052469/efe172b0cd58/BMRI2014-756078.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c1c/4052469/605d8de147a5/BMRI2014-756078.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c1c/4052469/efe172b0cd58/BMRI2014-756078.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c1c/4052469/605d8de147a5/BMRI2014-756078.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c1c/4052469/efe172b0cd58/BMRI2014-756078.002.jpg

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