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血管生成:子宫内膜异位症谜团的新线索。

Vasculogenesis: a new piece of the endometriosis puzzle.

机构信息

Institute for Clinical & Experimental Surgery, University of Saarland, Homburg/Saar, Germany.

出版信息

Hum Reprod Update. 2011 Sep-Oct;17(5):628-36. doi: 10.1093/humupd/dmr023. Epub 2011 May 17.

DOI:10.1093/humupd/dmr023
PMID:21586449
Abstract

BACKGROUND; Endometriosis is a complex disease with a multifactorial pathogenesis, which is crucially dependent on the development of new blood vessels. Based on the current literature, the present review highlights the fact that the neovascularization of endometriotic lesions is not only driven by angiogenesis, but also involves de novo formation of microvessels from circulating endothelial progenitor cells (EPCs). This process, termed post-natal vasculogenesis, is a characteristic of various pathogenic conditions, such as tumour growth and atherosclerosis, and typically comprises the activation, mobilization and recruitment of bone marrow-derived EPCs to the sites of tissue hypoxia. METHODS ; Literature searches were performed in PubMed, MEDLINE and ISI Web of Knowledge for publications focusing on vasculogenesis in the endometrium and endometriotic lesions. RESULTS ; Recent studies indicate that up to 37% of the microvascular endothelium of ectopic endometrial tissue originates from EPCs, partly controlled by the stromal-cell-derived factor-1/chemokine receptor type 4 axis. Accordingly, blockade of EPC recruitment effectively inhibits the formation of microvascular networks in developing endometriotic lesions, indicating that vasculogenesis represents an integral part of the pathogenesis of endometriosis. CONCLUSIONS ; The involvement of vasculogenesis in endometriosis may offer the exciting opportunity for the future establishment of novel diagnostic and therapeutic strategies for this frequent gynaecological disease.

摘要

背景

子宫内膜异位症是一种具有多因素发病机制的复杂疾病,其发病机制关键依赖于新血管的形成。基于目前的文献,本综述强调了这样一个事实,即子宫内膜异位症病变的新血管生成不仅受血管生成的驱动,还涉及循环内皮祖细胞(EPC)从头形成微血管。这个过程,称为出生后血管发生,是各种致病条件的特征,如肿瘤生长和动脉粥样硬化,通常包括骨髓来源的 EPC 的激活、动员和募集到组织缺氧部位。

方法

在 PubMed、MEDLINE 和 ISI Web of Knowledge 中进行文献检索,以获取关注子宫内膜和子宫内膜异位症中血管发生的出版物。

结果

最近的研究表明,多达 37%的异位子宫内膜组织的微血管内皮来源于 EPC,部分受基质细胞衍生因子-1/趋化因子受体 4 轴的控制。因此,EPC 募集的阻断有效地抑制了正在形成的子宫内膜异位症病变中小血管网络的形成,表明血管发生是子宫内膜异位症发病机制的一个组成部分。

结论

血管发生参与子宫内膜异位症可能为这种常见妇科疾病的未来建立新的诊断和治疗策略提供了令人兴奋的机会。

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Vasculogenesis: a new piece of the endometriosis puzzle.血管生成:子宫内膜异位症谜团的新线索。
Hum Reprod Update. 2011 Sep-Oct;17(5):628-36. doi: 10.1093/humupd/dmr023. Epub 2011 May 17.
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Endothelial progenitor cells contribute to the vascularization of endometriotic lesions.内皮祖细胞有助于子宫内膜异位症病灶的血管生成。
Am J Pathol. 2011 Jan;178(1):442-50. doi: 10.1016/j.ajpath.2010.11.037. Epub 2010 Dec 23.
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Role of endothelial progenitor cells in breast cancer angiogenesis: from fundamental research to clinical ramifications.内皮祖细胞在乳腺癌血管生成中的作用:从基础研究到临床意义。
Breast Cancer Res Treat. 2010 Feb;120(1):17-24. doi: 10.1007/s10549-009-0686-5. Epub 2009 Dec 24.
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Blocking of stromal cell-derived factor-1 reduces neoangiogenesis in human endometriosis lesions in a mouse model.基质细胞衍生因子-1 的阻断可减少小鼠模型中人子宫内膜异位症病变中的新生血管形成。
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The role of endothelial progenitor cells in tumour vasculogenesis.内皮祖细胞在肿瘤血管生成中的作用。
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Involvement of endothelial progenitor cells in tumor vascularization.内皮祖细胞在肿瘤血管生成中的作用。
Microvasc Res. 2010 May;79(3):217-23. doi: 10.1016/j.mvr.2010.01.007. Epub 2010 Jan 18.
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Fracture induced mobilization and incorporation of bone marrow-derived endothelial progenitor cells for bone healing.骨折诱导骨髓源性内皮祖细胞的动员与整合促进骨愈合。
J Cell Physiol. 2008 Apr;215(1):234-42. doi: 10.1002/jcp.21309.
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Matrix metalloproteinase-9 is essential for ischemia-induced neovascularization by modulating bone marrow-derived endothelial progenitor cells.基质金属蛋白酶-9通过调节骨髓来源的内皮祖细胞对缺血诱导的新生血管形成至关重要。
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Combined inhibition of vascular endothelial growth factor (VEGF), fibroblast growth factor and platelet-derived growth factor, but not inhibition of VEGF alone, effectively suppresses angiogenesis and vessel maturation in endometriotic lesions.联合抑制血管内皮生长因子(VEGF)、成纤维细胞生长因子和血小板衍生生长因子,而非单独抑制VEGF,可有效抑制子宫内膜异位症病灶中的血管生成和血管成熟。
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Cytometry A. 2008 Mar;73(3):186-93. doi: 10.1002/cyto.a.20480.

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