LaMarca Babbette, Cornelius Denise C, Harmon Ashlyn C, Amaral Lorena M, Cunningham Mark W, Faulkner Jessica L, Wallace Kedra
Department of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson, Mississippi; and Department of Obstetrics and Gynecology, University of Mississippi Medical Center, Jackson, Mississippi
Department of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson, Mississippi; and.
Am J Physiol Regul Integr Comp Physiol. 2016 Jul 1;311(1):R1-9. doi: 10.1152/ajpregu.00052.2016. Epub 2016 Apr 20.
Preeclampsia (PE) is a pregnancy-associated disorder that affects 5-8% of pregnancies and is a major cause of maternal, fetal, and neonatal morbidity and mortality. Hallmark characteristics of PE are new onset hypertension after 20 wk gestation with or without proteinuria, chronic immune activation, fetal growth restriction, and maternal endothelial dysfunction. However, the pathophysiological mechanisms that lead to the development of PE are poorly understood. Recent data from studies of both clinical and animal models demonstrate an imbalance in the subpopulations of CD4+ T cells and a role for these cells as mediators of inflammation and hypertension during pregnancy. Specifically, it has been proposed that the imbalance between two CD4+ T cell subtypes, regulatory T cells (Tregs) and T-helper 17 cells (Th17s), is involved in the pathophysiology of PE. Studies from our laboratory highlighting how this imbalance contributes to vasoactive factors, endothelial dysfunction, and hypertension during pregnancy will be discussed in this review. Therefore, the purpose of this review is to highlight hypertensive mechanisms stimulated by inflammatory factors in response to placental ischemia, thereby elucidating a role.
子痫前期（PE）是一种与妊娠相关的疾病，影响5%至8%的妊娠，是孕产妇、胎儿和新生儿发病和死亡的主要原因。PE的标志性特征是妊娠20周后新发高血压，伴或不伴有蛋白尿、慢性免疫激活、胎儿生长受限和母体血管内皮功能障碍。然而，导致PE发生发展的病理生理机制尚不清楚。来自临床和动物模型研究的最新数据表明，CD4+ T细胞亚群失衡，且这些细胞在妊娠期间作为炎症和高血压的介质发挥作用。具体而言，有人提出两种CD4+ T细胞亚型，即调节性T细胞（Tregs）和辅助性T细胞17（Th17s）之间的失衡参与了PE的病理生理过程。本综述将讨论我们实验室的研究，这些研究突出了这种失衡如何在妊娠期间导致血管活性因子、内皮功能障碍和高血压。因此，本综述的目的是强调炎症因子对胎盘缺血的反应所刺激的高血压机制，从而阐明其作用。
