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正常妊娠和自然流产中缺氧-蜕膜巨噬细胞调控轴。

A Hypoxia-Decidual Macrophage Regulatory Axis in Normal Pregnancy and Spontaneous Miscarriage.

机构信息

Laboratory for Reproductive Immunology, Hospital of Obstetrics and Gynecology, Fudan University, Shanghai 200080, China.

Department of Gynecology, Hospital of Obstetrics and Gynecology, Fudan University, Shanghai 200010, China.

出版信息

Int J Mol Sci. 2024 Sep 8;25(17):9710. doi: 10.3390/ijms25179710.

DOI:10.3390/ijms25179710
PMID:39273657
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11395248/
Abstract

The significance of hypoxia at the maternal-fetal interface is proven to be self-explanatory in the context of pregnancy. During the first trimester, low oxygen conditions play a crucial role in processes such as angiogenesis, trophoblast invasion and differentiation, and immune regulation. Recently, there has been increasing research on decidual macrophages, which contribute to the maintenance of immune tolerance, placental and fetal vascular development, and spiral artery remodeling, to investigate the effects of hypoxia on their biological behaviors. On these grounds, this review describes the dynamic changes in oxygen levels at the maternal-fetal interface throughout gestation, summarizing current knowledge on how the hypoxic environment sustains a successful pregnancy by regulating retention, differentiation and efferocytosis of decidual macrophages. Additionally, we explore the relationship between spontaneous miscarriages and an abnormal hypoxia-macrophage axis, shedding light on the underlying mechanisms. However, further studies are essential to elucidate these pathways in greater detail and to develop targeted interventions that could improve pregnancy outcomes.

摘要

母体-胎儿界面缺氧的意义在妊娠背景下不言而喻。在孕早期,低氧条件在血管生成、滋养细胞侵袭和分化以及免疫调节等过程中发挥着关键作用。最近,越来越多的研究集中在蜕膜巨噬细胞上,这些细胞有助于维持免疫耐受、胎盘和胎儿血管发育以及螺旋动脉重塑,以研究缺氧对其生物学行为的影响。基于这些原因,本综述描述了妊娠期间母体-胎儿界面氧气水平的动态变化,总结了目前关于缺氧环境如何通过调节蜕膜巨噬细胞的保留、分化和吞噬作用来维持成功妊娠的知识。此外,我们探讨了自然流产与异常缺氧-巨噬细胞轴之间的关系,揭示了潜在的机制。然而,还需要进一步的研究来更详细地阐明这些途径,并开发出可以改善妊娠结局的靶向干预措施。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9685/11395248/7f62eb5f6482/ijms-25-09710-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9685/11395248/089b67b0269f/ijms-25-09710-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9685/11395248/7f62eb5f6482/ijms-25-09710-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9685/11395248/089b67b0269f/ijms-25-09710-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9685/11395248/7f62eb5f6482/ijms-25-09710-g002.jpg

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本文引用的文献

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JPT2 Affects Trophoblast Functions and Macrophage Polarization and Metabolism, and Acts as a Potential Therapeutic Target for Recurrent Spontaneous Abortion.JPT2影响滋养层细胞功能、巨噬细胞极化和代谢,并作为复发性自然流产的潜在治疗靶点。
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FKBP5 regulates trophoblast-macrophage crosstalk in recurrent spontaneous abortion through PI3K/AKT and NF-κB signaling pathways.FKBP5 通过 PI3K/AKT 和 NF-κB 信号通路调节复发性自然流产中滋养层细胞与巨噬细胞的相互作用。
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Fetal Oxygenation from the 23rd to the 36th Week of Gestation Evaluated through the Umbilical Cord Blood Gas Analysis.通过脐血血气分析评估妊娠 23 周至 36 周时的胎儿氧合情况。
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PlGF/FLT-1 deficiency leads to reduced STAT3-C/EBPβ signaling and aberrant polarization in decidual macrophages during early spontaneous abortion.PlGF/FLT-1 缺乏导致早期自发性流产时蜕膜巨噬细胞中 STAT3-C/EBPβ 信号转导减少和异常极化。
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