遗传性出血性毛细血管扩张症：血管生长和扩张的模型 - Suppr

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超能文献

Hereditary hemorrhagic telangiectasia: A model for blood vessel growth and enlargement.

作者信息

Jacobson B S

机构信息

Department of Biochemistry and Molecular Biology, University of Massachusetts, Amherst, Massachusetts 01003, USA.

出版信息

Am J Pathol. 2000 Mar;156(3):737-42. doi: 10.1016/S0002-9440(10)64939-5.

DOI:10.1016/S0002-9440(10)64939-5

PMID:10702387

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1876865/

Abstract

摘要

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Hereditary hemorrhagic telangiectasia: A model for blood vessel growth and enlargement.

Am J Pathol. 2000 Mar;156(3):737-42. doi: 10.1016/S0002-9440(10)64939-5.

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本文引用的文献

Endoglin expression is reduced in normal vessels but still detectable in arteriovenous malformations of patients with hereditary hemorrhagic telangiectasia type 1.

Am J Pathol. 2000 Mar;156(3):911-23. doi: 10.1016/S0002-9440(10)64960-7.

Heterogeneity of the angiogenic response induced in different normal adult tissues by vascular permeability factor/vascular endothelial growth factor.

Lab Invest. 2000 Jan;80(1):99-115. doi: 10.1038/labinvest.3780013.

Endoglin, an ancillary TGFbeta receptor, is required for extraembryonic angiogenesis and plays a key role in heart development.

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Identification of hereditary hemorrhagic telangiectasia type 1 in newborns by protein expression and mutation analysis of endoglin.

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Circ Res. 1999 Nov 12;85(10):877-9. doi: 10.1161/01.res.85.10.877.

Expression analysis of four endoglin missense mutations suggests that haploinsufficiency is the predominant mechanism for hereditary hemorrhagic telangiectasia type 1.

Hum Mol Genet. 1999 Nov;8(12):2171-81. doi: 10.1093/hmg/8.12.2171.

Positive and negative regulation of the myeloid dendritic cell lineage.

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Circ Res. 1999 Aug 6;85(3):221-8. doi: 10.1161/01.res.85.3.221.

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