Department of Medicine, Division of Renal Diseases and Hypertension, George Washington University School of Medicine and Health Sciences, Washington, DC, USA.
Semin Nephrol. 2011 Jan;31(1):33-46. doi: 10.1016/j.semnephrol.2010.10.004.
Preeclampsia, a hypertensive disorder peculiar to pregnancy, is a systemic syndrome that appears to originate in the placenta and is characterized by widespread maternal endothelial dysfunction. Until recently, the molecular pathogenesis of phenotypic preeclampsia was largely unknown, but recent observations support the hypothesis that altered expression of placental anti-angiogenic factors are responsible for the clinical manifestations of the disease. Soluble Flt1 and soluble endoglin, secreted by the placenta, are increased in the maternal circulation weeks before the onset of preeclampsia. These anti-angiogenic 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 as of 2011 the role of angiogenic proteins in early placental vascular development was starting to be explored. The data linking angiogenic factors to preeclampsia have exciting clinical implications, and likely will transform the detection and treatment of preeclampsia.
子痫前期是一种妊娠特有的高血压疾病，是一种全身性综合征，似乎起源于胎盘，其特征是广泛的母体血管内皮功能障碍。直到最近，表型子痫前期的分子发病机制在很大程度上还不清楚，但最近的观察结果支持这样一种假设，即胎盘抗血管生成因子的表达改变是疾病临床表现的原因。由胎盘分泌的可溶性 Flt1 和可溶性内格林在子痫前期发作前数周就会在母体循环中增加。这些抗血管生成因子会导致全身血管内皮功能障碍，从而导致高血压、蛋白尿和子痫前期的其他全身表现。这些致病因子胎盘调节紊乱的分子基础尚不清楚，截至 2011 年，血管生成蛋白在早期胎盘血管发育中的作用才刚刚开始被探索。将血管生成因子与子痫前期联系起来的数据具有令人兴奋的临床意义，可能会改变子痫前期的检测和治疗。
