子痫前期
胎盘
发病机制
内皮糖蛋白
蛋白尿
内皮功能障碍
怀孕
医学
血管生成
胎儿
免疫学
内科学
生物信息学
生物
肾
干细胞
遗传学
川地34
作者
Sharon E. Maynard,Franklin H. Epstein,S. Ananth Karumanchi
标识
DOI:10.1146/annurev.med.59.110106.214058
摘要
Preeclampsia is a systemic syndrome of pregnancy that originates in the placenta and is characterized by widespread maternal endothelial dysfunction. Until recently, the molecular pathogenesis of preeclampsia was largely unknown, but recent work suggests a key role for altered expression of placental antiangiogenic factors. Soluble Flt1 and soluble endoglin, secreted by the placenta, are increased in the maternal circulation weeks before the onset of preeclampsia. These antiangiogenic factors produce systemic endothelial dysfunction, resulting in hypertension, proteinuria, and the other systemic manifestations of preeclampsia. The molecular basis for placental dysregulation of these pathogenic factors remains unknown, and the role of angiogenic proteins in early placental vascular development is just beginning to be explored. These discoveries have exciting clinical implications and are likely to transform the detection and treatment of preeclampsia in the future.
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