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作 者:曾婵娟 张卫社[1] 裴琛琳[1] Zeng Chanjuan;Zhang Weishe;Pei Chenlin(Department of Obstetrics and Gynecology,Xiangya Hospital of Central South University,Hunan Engineering Research Center of Early Life Development and Disease Prevention,Changsha 410008,China)
机构地区:[1]中南大学湘雅医院产科,湖南省“早期生命发育与疾病防控”工程研究中心,长沙410008
出 处:《中华围产医学杂志》2019年第10期735-739,共5页Chinese Journal of Perinatal Medicine
摘 要:胎盘源性妊娠并发症(placenta-mediated pregnancy complication,PMPC)是一组由于妊娠早期滋养细胞浸润不足、子宫螺旋动脉重铸障碍所导致的母胎并发症,主要包括子痫前期、胎儿生长受限和复发性流产等,可导致不良母胎结局,影响母儿远期健康。PMPC的具体分子机制尚未阐明。内分泌性血管内皮生长因子(endocrine gland-derived vascular endothelial growth factor, EG-VEGF)特异性高表达于胎盘组织,是一种调节胎盘发育的关键因子。该因子通过促进血管发生及抑制滋养细胞迁移浸润,在正常妊娠胎盘的形成过程中起重要作用。同时EG-VEGF分泌异常与PMPC的发生发展密切相关。本文综述了EG-VEGF的相关研究进展,以期为认识PMPC发病机制并早期预测PMPC提供新的分子靶点。Placenta-mediated pregnancy complication (PMPC),including preeclampsia, fetal growth restriction and recurrent pregnancy loss, is caused by inadequate trophoblast invasion and abnormal remodeling of maternal spiral arteries in early pregnancy, resulting in adverse perinatal outcomes and affecting the long-term maternal and child health. However, the molecular mechanisms of PMPC remain unclear. Endocrine gland-derived vascular endothelial growth factor (EG-VEGF) is highly expressed in human placenta and plays an important role in the development of a normal placenta through promoting placental angiogenesis and inhibiting trophoblast migration and invasion. EG-VEGF dysregulation is closely related to the pathogenesis of PMPC. This review described recent advances in EG-VEGF for better understanding of the underlying mechanism of PMPC and providing a potential biomarker for early diagnosis of PMPC.
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