不明原因绒毛炎致滋养细胞凋亡在胎儿生长受限发病中的作用

doi:10.12280/gjfckx.20220067

摘要/Abstract

摘要：

胎儿生长受限（fetal growth restriction,FGR）是产科常见并发症,临床上与多种围生儿不良结局有关。目前FGR发病机制不明,胎盘功能不全被认为是导致FGR发生的主要原因之一。不明原因绒毛炎（villitis of unknown etiology,VUE）是妊娠中、晚期常见的原因不明的非感染性胎盘炎症改变,以母体T细胞浸润绒毛间质和炎性细胞因子失调为特征。正常妊娠时滋养细胞有适度凋亡,VUE时增加的CD8⁺T淋巴细胞及霍夫鲍尔（Hofbauer）细胞活化后可分泌多种炎性细胞因子,促进滋养细胞凋亡,而滋养细胞凋亡可致胎盘发育不良、绒毛血管闭塞和胎盘血流灌注不足等,导致胎盘功能不全,与FGR的发病关系密切。目前VUE导致胎盘滋养细胞凋亡在FGR发生中的机制尚不明确。综述VUE时滋养细胞凋亡在FGR发病中的作用。

关键词: 不明原因绒毛炎, 胎儿生长迟缓, 滋养层, 细胞凋亡, 妊娠结局

Abstract:

Fetal growth restriction (FGR) is a common obstetric complications associated with many perinatal adverse pregnancy outcomes. The pathogenesis of FGR is still unknown at present,and placental insufficiency is considered to be one of the main causes of FGR. Villitis of unknown etiology (VUE) is a common non-infectious placental inflammatory change of unknown origin in the middle and late trimester, characterized by maternal T cells infiltration into the villus stroma and inflammatory cytokine dysregulation. There is moderate apoptosis of trophoblast cells in normal pregnancy, while in VUE, the increased CD8⁺T lymphocytes and Hofbauer cells can secrete a variety of cytokines after activation,which can promote the apoptosis of trophoblast cells, resulting in placental dysplasia, fetal thrombotic vasculopathy, and placental hypoperfusion. These will lead to placental insufficiency, which is associated with fetal growth restriction closely. However, the mechanism of VUE inducing apoptosis of placental trophoblast cells in the occurrence of FGR remains unclear. This article reviews the research progress of trophoblast apoptosis and FGR during VUE briefly.

Key words: Villitis of unknown etiology, Fetal growth retardation, Trophoblasts, Apoptosis, Pregnancy outcome

瞿琳, 周欣, 孙丽洲. 不明原因绒毛炎致滋养细胞凋亡在胎儿生长受限发病中的作用[J]. 国际妇产科学杂志, 2022, 49(4): 415-419.

QU Lin, ZHOU Xin, SUN Li-zhou. Research Progress of Trophoblast Apoptosis Induced by Villitis of Unknown Etiology in Fetal Growth Restriction[J]. Journal of International Obstetrics and Gynecology, 2022, 49(4): 415-419.

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