Foidart Jean-Michel, Noël Agnès, Chantraine Frédéric, Lorquet Sophie, Petit Philippe, Munaut Carine, Berndt Sarah, Pequeux Christel, Schaaps Jean-Pierre
Gynécologie-Obstétrique, Université de Liège, Hôpital de la Citadelle, 1 boulevard du 12e ligne, B-4000 Liège, Belgique.
Bull Acad Natl Med. 2009 May;193(5):1059-64; discussion 1064-6, 1067-8.
Preeclampsia, a pregnancy-specific syndrome characterized by hypertension, edema and proteinuria, resolves spontaneously on placental delivery. Its pathogenesis is thought to involve placental hypoxia, which leads to maternal vascular dysfunction through increased placental release of anti-angiogenic factors such as the soluble form of VEGF receptor-1 (VEGFR1). VEGFR1 binds VEGF and PIGF, which are also produced by villous trophoblastic cells. In the absence of VEGF and PIGF in the maternal circulation, endothelial dysfunction occurs in several vascular territories (liver, kidneys, brain, heart, lungs, etc.). In experimental models, sVEGFR1 not only has an anti-angiogenic action but also augments endothelial expression of NO synthase through intracellular transduction. When NO production is increased, pericytes and perivascular smooth muscle cells are recruited and their adhesion to endothelial cells is strongly stimulated. This can hinder both trophoblast invasion and increase uteroplacental flow during preeclampsia.
子痫前期是一种特定于妊娠的综合征，其特征为高血压、水肿和蛋白尿，在胎盘娩出后会自发缓解。其发病机制被认为涉及胎盘缺氧，这会通过胎盘释放增加的抗血管生成因子（如可溶性血管内皮生长因子受体-1（VEGFR1））导致母体血管功能障碍。VEGFR1结合血管内皮生长因子（VEGF）和胎盘生长因子（PIGF），它们也由绒毛滋养层细胞产生。在母体循环中缺乏VEGF和PIGF时，会在多个血管区域（肝脏、肾脏、大脑、心脏、肺等）发生内皮功能障碍。在实验模型中，可溶性VEGFR1不仅具有抗血管生成作用，还通过细胞内转导增强一氧化氮合酶的内皮表达。当一氧化氮生成增加时，会募集周细胞和血管周围平滑肌细胞，并强烈刺激它们与内皮细胞的粘附。这在子痫前期既会阻碍滋养层侵袭，又会增加子宫胎盘血流。
