What causes endothelial cell activation in preeclamptic women?
What causes endothelial cell activation in preeclamptic women?
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DOI：
10.2353/ajpath.2006.060713
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发表时间：
2006-10
期刊：
影响因子：
--
通讯作者：
S. Walsh
中科院分区：
文献类型：
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作者：
S. Walsh
先兆子痫是一种妊娠期高血压疾病，是胎儿和母亲发病率和死亡率的主要原因。它与蛋白尿、病理性水肿、凝血异常、子宫胎盘血流量减少和宫内生长受限有关。先兆子痫的原因尚不清楚，但有充分的证据表明，它与内皮细胞活化和功能障碍有关。许多研究者已经证明了先兆子痫妇女的内皮细胞活化标志物。内皮激活的指标包括血管性血友病因子、内皮素、可溶性血管细胞粘附分子、血栓调节蛋白和细胞纤连蛋白的循环水平升高以及生长因子活性升高。1，2内皮细胞功能障碍的最重要指标可能是前列环素的血浆和尿液水平降低，因为内皮细胞是前列环素的主要来源。3 -5先兆子痫妇女血液中存在的因子引起内皮细胞活化。例如，与正常妊娠妇女的血浆或血清相比，内皮细胞暴露于先兆子痫妇女的血浆或血清会导致核因子-κB活化，细胞间粘附分子-1和血管细胞粘附分子-1表达增加。6，7抗氧化剂治疗可预防这些效应，因此氧化应激似乎介导了血浆因子的作用。问题仍然是什么因素或因子存在于先兆子痫妇女的血液中导致内皮细胞活化。到目前为止，已经提出了一些可能的候选人。
Preeclampsia is a hypertensive disorder of pregnancy and a leading cause of fetal and maternal morbidity and mortality. It is associated with proteinuria, pathological edema, coagulation abnormalities, reduced uteroplacental blood flow, and intrauterine growth restriction. The cause of preeclampsia is not known, but there is good evidence that it is associated with endothelial cell activation and dysfunction. Many investigators have demonstrated markers of endothelial cell activation in women with preeclampsia. Indicators of endothelial activation include increased circulating levels of von Willebrand factor, endothelin, soluble vascular cell adhesion molecule, thrombomodulin, and cellular fibronectin as well as increased growth factor activity.1,2 Perhaps the most important indicator of endothelial cell dysfunction is decreased plasma and urinary levels of prostacyclin, because the endothelium is the main source of prostacyclin.3–5 Factors present in the blood of preeclamptic women cause endothelial cell activation. For example, exposure of endothelial cells to plasma or serum from preeclamptic women causes activation of nuclear factor-κB and increased expression of intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 compared with plasma or serum from normal pregnant women.6,7 Treatment with antioxidants prevents these effects, so oxidative stress appears to mediate the effects of plasma factors. The question remains what factor or factors present in the blood of preeclamptic women causes endothelial cell activation. To date, a number of possible candidates have been suggested.