Saito Shigeru, Nakashima Akitoshi
Department of Obstetrics and Gynecology, University of Toyama, Toyama, Japan.
Department of Obstetrics and Gynecology, University of Toyama, Toyama, Japan.
J Reprod Immunol. 2014 Mar;101-102:80-88. doi: 10.1016/j.jri.2013.06.002. Epub 2013 Aug 2.
Shallow trophoblast invasion and impaired vascular remodeling of spiral arteries have been recognized in early-onset preeclampsia. Placentation and vascular remodeling are multistep processes, and hypoxia, placental oxidative stress, excessive or atypical maternal immune response to trophoblasts, exaggerated inflammation, and increased production of anti-angiogenic factors such as the soluble form of the vascular endothelial growth factor (VEGF) receptor (sFlt-1) and soluble endoglin (sENG) may play a role in poor placentation in preeclampsia. Recent findings suggest that autophagy plays an important role in extravillous trophoblast (EVT) invasion and vascular remodeling under hypoxia, and sENG inhibits EVT invasion and vascular remodeling by the inhibition of autophagy under hypoxic conditions. In this review, we discuss the relationship between inadequate autophagy and poor placentation in preeclampsia.
早发型子痫前期已被证实存在滋养层细胞浸润浅及螺旋动脉血管重塑受损的情况。胎盘形成和血管重塑是多步骤过程，而缺氧、胎盘氧化应激、母体对滋养层细胞过度或非典型的免疫反应、炎症反应过度以及抗血管生成因子如血管内皮生长因子（VEGF）受体的可溶性形式（sFlt-1）和可溶性内皮糖蛋白（sENG）产生增加可能在子痫前期胎盘形成不良中起作用。最近的研究结果表明，自噬在缺氧条件下的绒毛外滋养层（EVT）浸润和血管重塑中起重要作用，并且sENG在缺氧条件下通过抑制自噬来抑制EVT浸润和血管重塑。在本综述中，我们讨论了子痫前期自噬不足与胎盘形成不良之间的关系。
