Faculty of Medicine, Catholic University of Leuven, Leuven, Belgium.
Division of Biomedical Sciences, Warwick Medical School, Coventry, United Kingdom.
Am J Obstet Gynecol. 2019 Sep;221(3):219-226. doi: 10.1016/j.ajog.2019.01.239. Epub 2019 Feb 6.
We explore the potential role of the endothelial lining of uteroplacental arteries in the pathogenesis of preeclampsia, a severe pregnancy disorder characterized by incomplete invasion of the uterine vasculature by extravillous trophoblast and angiogenic imbalance. In normal pregnancy, the endothelium disappears progressively from the uteroplacental arteries and is replaced by trophoblast and deposition of fibrofibrinoid structure, underpinning the so-called physiological transformation of uterine spiral arteries. We hypothesize that partial persistence of the endothelium, albeit injured, initiates a chain of events leading to the emergence of preeclampsia in 3 sequential stages. The first stage results in retention of the endothelium in uteroplacental arteries secondary to incomplete physiological transformation of the vessels. Consequently, the uteroplacental vessels are reactive to pathological cues, which drives local arteriopathy. The second stage starts with progressive reduction in uteroplacental blood flow, generating oxidative stress in the whole placenta, and heightened maternal inflammation in response to circulating trophoblastic debris. In the third stage, generalized endotheliosis causes systemic angiogenic imbalance, hypertension, and other clinical manifestation of preeclampsia.
我们探讨了内皮衬里在胎盘血管发病机制中的潜在作用子痫前期，这是一种严重的妊娠疾病，其特征是绒毛外滋养细胞不完全侵入子宫血管和血管生成失衡。在正常妊娠中，内皮细胞逐渐从胎盘血管中消失，被滋养细胞和纤维蛋白样结构取代，支撑着所谓的子宫螺旋动脉的生理转化。我们假设内皮细胞的部分持续存在，尽管受到损伤，会引发一系列事件，导致子痫前期在 3 个连续阶段出现。第一阶段导致胎盘血管的不完全生理转化导致胎盘血管中内皮细胞的保留。因此，胎盘血管对病理信号有反应，导致局部血管疾病。第二阶段始于胎盘血流逐渐减少，整个胎盘产生氧化应激，以及母体对循环滋养细胞碎片的炎症反应加剧。在第三阶段，全身性内皮细胞增多症导致全身血管生成失衡、高血压和子痫前期的其他临床表现。
