Preeclampsia: the role of persistent endothelial cells in uteroplacental arteries
Preeclampsia: the role of persistent endothelial cells in uteroplacental arteries
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DOI：
10.1016/j.ajog.2019.01.239
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发表时间：
2019-09-01
影响因子：
9.8
通讯作者：
Benagiano, Giuseppe
中科院分区：
文献类型：
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作者：
Brosens, Ivo;Brosens, Jan J.;Benagiano, Giuseppe
我们探讨了子宫胎盘动脉内皮层在先兆子痫发病机制中的潜在作用，先兆子痫是一种严重的妊娠性疾病，其特征是绒毛外滋养层不完全侵入子宫脉管系统和血管生成失衡。在正常妊娠中，内皮逐渐从子宫胎盘动脉消失，并被滋养层和纤维蛋白样结构的沉积所取代，支撑所谓的子宫螺旋动脉的生理转变。我们假设，尽管内皮细胞受到损伤，但部分持续存在会引发一系列事件，导致子痫前期在三个连续阶段的出现。第一阶段导致内皮保留在子宫胎盘动脉中，继发于血管不完全的生理转变。因此，子宫胎盘血管会对病理信号产生反应，从而导致局部动脉病变。第二阶段开始时，子宫胎盘血流量逐渐减少，在整个胎盘中产生氧化应激，并加剧母体对循环滋养层碎片的炎症反应。第三阶段，广泛性内皮增生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。
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.