Emerging role for dysregulated decidualization in the genesis of preeclampsia.
Emerging role for dysregulated decidualization in the genesis of preeclampsia.
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DOI：
10.1016/j.placenta.2017.06.005
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发表时间：
2017-12
期刊：
影响因子：
3.8
通讯作者：
Post Uiterweer ED
中科院分区：
文献类型：
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作者：
Conrad KP;Rabaglino MB;Post Uiterweer ED
在正常的人类胎盘形成中，滋养层细胞侵袭子宫和随后的螺旋动脉重建依赖于胎儿滋养层细胞和母体蜕膜、子宫肌层、免疫细胞和子宫壁血管细胞之间的合作。因此，从理论上讲，这些细胞类型中的任何一个或几个的功能异常都会损害胎盘形成，从而导致先兆子痫的发生。由于滋养层细胞的侵袭和螺旋动脉的重建发生在妊娠的前半期，分娩后胎儿胎盘和母体蜕膜组织的分子病理学可能不能提供关于几个月前发生的胎盘损害的起源的信息。因此，在这篇综述中，我们主要关注支持这一概念的新的前瞻性证据，即在分泌晚期和妊娠早期，子宫内膜成熟不足或缺陷，即蜕膜前和蜕膜前，可能与子痫前期的发生有关。第一批直接支持这一概念的前瞻性获得的数据，出人意料地在对5个月后发展为先兆子痫的妇女在怀孕早期获得的绒毛样本(CVS)的转录分析中揭示出来。其他支持性证据来自对子宫动脉指数较高的妇女选择性终止妊娠早期蜕膜中自然杀伤细胞的研究，子宫动脉指数是滋养层侵袭不足的替代物。最后，先兆子痫患者妊娠早期，蜕膜基质细胞分泌的循环胰岛素生长因子结合蛋白-1减少。在总结这篇综述时，我们建议进一步进行前瞻性设计的研究，以证实子痫前期子宫内膜前驱因素的概念。这些研究还可以确定患先兆子痫风险增加的妇女，揭示蜕膜缺陷或缺陷(前)的分子机制，并导致旨在改善(前)蜕膜化的预防性策略，从而降低先兆子痫的发展风险。
In normal human placentation, uterine invasion by trophoblast cells and subsequent spiral artery remodeling depend on cooperation among fetal trophoblasts and maternal decidual, myometrial, immune and vascular cells in the uterine wall. Therefore, aberrant function of anyone or several of these cell-types could theoretically impair placentation leading to the development of preeclampsia. Because trophoblast invasion and spiral artery remodeling occur during the first half of pregnancy, the molecular pathology of fetal placental and maternal decidual tissues following delivery may not be informative about the genesis of impaired placentation, which transpired months earlier. Therefore, in this review, we focus on the emerging prospective evidence supporting the concept that deficient or defective endometrial maturation in the late secretory phase and during early pregnancy, i.e., pre-decidualization and decidualization, respectively, may contribute to the genesis of preeclampsia. The first prospectively-acquired data directly supporting this concept were unexpectedly revealed in transcriptomic analyses of chorionic villous samples (CVS) obtained during the first trimester of women who developed preeclampsia 5 months later. Additional supportive evidence arose from investigations of Natural Killer cells in first trimester decidua from elective terminations of women with high resistance uterine artery indices, a surrogate for deficient trophoblast invasion. Last, circulating insulin growth factor binding protein-1, which is secreted by decidual stromal cells was decreased during early pregnancy in women who developed preeclampsia. We conclude this review by making recommendations for further prospectively-designed studies to corroborate the concept of endometrial antecedents of preeclampsia. These studies could also enable identification of women at increased risk for developing preeclampsia, unveil the molecular mechanisms of deficient or defective (pre)decidualization, and lead to preventative strategies designed to improve (pre)decidualization, thereby reducing risk for preeclampsia development.
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影响因子：
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作者：
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通讯作者：
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DOI：
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发表时间：
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DOI：
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发表时间：
2012-03-13
期刊：
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影响因子：
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作者：
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