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.

中文翻译：

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子痫前期和血管生成失衡。

子痫前期是起源于胎盘的全身性妊娠综合征，其特征在于广泛的母体内皮功能障碍。直到最近，先兆子痫的分子发病机理仍是未知的，但是最近的工作表明胎盘抗血管生成因子表达改变的关键作用。子痫前期发病前几周，胎盘分泌的可溶性Flt1和可溶性内皮糖蛋白增加。这些抗血管生成因子产生全身性内皮功能障碍，导致高血压，蛋白尿和先兆子痫的其他全身性表现。这些致病因素的胎盘失调的分子基础仍是未知的，而血管生成蛋白在胎盘早期血管发育中的作用才刚刚开始被探索。