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子痫前期的起源:从蜕膜“高氧”到晚期缺氧。

The origin of pre-eclampsia: from decidual "hyperoxia" to late hypoxia.

机构信息

Department of Clinical Sciences, Section of Women's Health Sciences, Università Politecnica Marche, Ancona, Italy.

出版信息

Med Hypotheses. 2010 Jul;75(1):38-46. doi: 10.1016/j.mehy.2010.01.024. Epub 2010 Feb 18.

DOI:10.1016/j.mehy.2010.01.024
PMID:20171021
Abstract

Normal gestation implants on a relatively hypoxic deciduas so that trophoblast deeply invades endometrium and angiogenesis seeks for oxygen supply. If implantation occurs before those hypoxic conditions occur, trophoblast invasion is defective, due to the relatively high oxygen tension in the decidual environment, laying the foundations for subsequent pre-eclampsia.

摘要

正常妊娠时,胎盘会植入相对缺氧的蜕膜中,使滋养细胞深入侵袭子宫内膜并寻找血管生成以获取氧气供应。如果植入发生在这些缺氧条件出现之前,由于蜕膜环境中的氧气张力相对较高,滋养细胞的侵袭会出现缺陷,为随后的子痫前期奠定基础。

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Hypoxia down-regulates placenta growth factor, whereas fetal growth restriction up-regulates placenta growth factor expression: molecular evidence for "placental hyperoxia" in intrauterine growth restriction.缺氧会下调胎盘生长因子,而胎儿生长受限会上调胎盘生长因子的表达:宫内生长受限中“胎盘高氧”的分子证据。
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[Significance of the hypoxic syndrome in the pathogenesis of diseases of the pregnant mother and child].[缺氧综合征在孕产妇和儿童疾病发病机制中的意义]
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