George Eric M, Granger Joey P
Department of Physiology and Biophysics and the Center for Excellence in Cardiovascular-Renal Research, University of Mississippi Medical Center, 2500 N. State Street, Jackson, MS 39216, USA.
Expert Rev Obstet Gynecol. 2010 Sep 1;5(5):557-566. doi: 10.1586/eog.10.45.
Preeclampsia, characterized by new-onset gestational hypertension and proteinuria, is a common and serious complication of pregnancy. Evidence from both animal and human studies has implicated placental ischemia and hypoxia as a central causative factor in the etiology of the disorder. The ischemic placenta in turn initiates a cascade of secondary effector mechanisms, including altered proangiogenic and antiangiogenic factor balance, increase in maternal oxidative stress and endothelial and immunological dysfunction. The full elucidation of these mechanisms will hopefully lead to a more complete understanding of the etiology of preeclampsia and lead to successful therapeutic intervention through the targeted disruption of new and novel pathways.
子痫前期以新发妊娠高血压和蛋白尿为特征,是一种常见且严重的妊娠并发症。动物和人体研究的证据均表明胎盘缺血和缺氧是该疾病病因中的核心致病因素。缺血的胎盘继而引发一系列继发性效应机制,包括促血管生成因子和抗血管生成因子平衡改变、母体氧化应激增加以及内皮和免疫功能障碍。对这些机制的全面阐释有望带来对子痫前期病因更完整的理解,并通过针对性地阻断新的途径实现成功的治疗干预。