Soluble fms-like tyrosine kinase 1 and soluble endoglin are elevated circulating anti-angiogenic factors in pre-eclampsia

被引:20
作者
Liu, Zhen [1 ,2 ]
Afink, Gijs B. [3 ]
ten Dijke, Peter [1 ,2 ]
机构
[1] Leiden Univ, Med Ctr, Dept Mol Cell Biol, NL-2300 RC Leiden, Netherlands
[2] Leiden Univ, Med Ctr, Ctr Biomed Genet, NL-2300 RC Leiden, Netherlands
[3] Univ Amsterdam, Acad Med Ctr, Reprod Biol Lab, NL-1105 AZ Amsterdam, Netherlands
关键词
Angiogenesis; Endothelial dysfunction; Pre-eclampsia; sFlt1; Soluble endoglin; TGF-beta; VEGF; ENDOTHELIAL-GROWTH-FACTOR; REDUCED UTERINE PERFUSION; BETA BINDING-PROTEIN; FACTOR RECEPTOR-1; TGF-BETA; SIGNAL-TRANSDUCTION; CELL PROLIFERATION; CRYSTAL-STRUCTURE; HUMAN PLACENTA; PREGNANT RATS;
D O I
10.1016/j.preghy.2012.06.003
中图分类号
R71 [妇产科学];
学科分类号
100211 ;
摘要
Pre-eclampsia, characterized by hypertension and proteinuria, affects approximately 3-5% of all pregnancies worldwide and is a major cause of maternal and fetal morbidity and mortality. Maternal endothelial dysfunction is associated with disease pathogenesis. Recently, reports have shown that elevated levels of circulating soluble fms-like tyrosine kinase 1 [sFlt1] and soluble endoglin [sEng] are associated with pre-eclampsia. Flt1 is a receptor for vascular endothelial growth factor receptor [VEGF], whereas endoglin [Eng] is an auxiliary receptor for transforming growth factor-beta [TGF-beta] super-family members. Both signaling pathways modulate angiogenesis and are involved in vascular homeostasis. Increased levels of sFlt1 and sEng dysregulate VEGF and TGF-beta signaling respectively, resulting in endothelial dysfunction of maternal blood vessels. This review summarizes our current knowledge of Flt1 and endoglin and soluble forms in pre-eclampsia. Furthermore, it highlights the predictive and early-screening value of circulating levels of sFlt1 and sEng for the risk of developing pre-eclampsia. (C) 2012 International Society for the Study of Hypertension in Pregnancy. Published by Elsevier B.V. All rights reserved.
引用
收藏
页码:358 / 367
页数:10
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