Department of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson, Mississippi.
Department of Obstetrics and Gynecology, University of Mississippi Medical Center, Jackson, Mississippi.
Kidney360. 2022 Aug 12;3(10):1785-1794. doi: 10.34067/KID.0001282022. eCollection 2022 Oct 27.
Preeclampsia (PE), new-onset hypertension during pregnancy, affects up to 10% of pregnancies worldwide. Despite being the leading cause of maternal and fetal morbidity and mortality, PE has no cure beyond the delivery of the fetal-placental unit. Although the exact pathogenesis of PE is unclear, there is a strong correlation between chronic immune activation; intrauterine growth restriction; uterine artery resistance; dysregulation of the renin-angiotensin system. Which contributes to renal dysfunction; and the resulting hypertension during pregnancy. The genesis of PE is thought to begin with insufficient trophoblast invasion leading to reduced spiral artery remodeling, resulting in decreased placental perfusion and thereby causing placental ischemia. The ischemic placenta releases factors that shower the endothelium and contribute to peripheral vasoconstriction and chronic immune activation and oxidative stress. Studies have shown imbalances in proinflammatory and anti-inflammatory cell types in women with PE and in animal models used to examine mediators of a PE phenotype during pregnancy. T cells, B cells, and natural killer cells have all emerged as potential mediators contributing to the production of vasoactive factors, renal and endothelial dysfunction, mitochondrial dysfunction, and hypertension during pregnancy. The chronic immune activation seen in PE leads to a higher risk for other diseases, such as cardiovascular disease, CKD, dementia during the postpartum period, and PE during a subsequent pregnancy. The purpose of this review is to highlight studies demonstrating the role that different lymphoid cell populations play in the pathophysiology of PE. Moreover, we will discuss treatments focused on restoring immune balance or targeting specific immune mediators that may be potential strategies to improve maternal and fetal outcomes associated with PE.
子痫前期（PE），即妊娠期间新发高血压，影响全球多达 10%的妊娠。尽管它是孕产妇和胎儿发病率和死亡率的主要原因，但除了分娩胎儿胎盘单位外，没有治愈方法。尽管 PE 的确切发病机制尚不清楚，但慢性免疫激活；宫内生长受限；子宫动脉阻力；肾素-血管紧张素系统失调之间存在很强的相关性。这会导致肾功能障碍；以及怀孕期间随之而来的高血压。PE 的发生被认为始于滋养细胞侵袭不足，导致螺旋动脉重塑减少，从而导致胎盘灌注减少，从而导致胎盘缺血。缺血的胎盘释放出作用于内皮的因子，导致外周血管收缩和慢性免疫激活和氧化应激。研究表明，PE 妇女和用于检查妊娠期间 PE 表型介体的动物模型中存在促炎和抗炎细胞类型的失衡。T 细胞、B 细胞和自然杀伤细胞都已成为潜在的介体，有助于血管活性因子、肾和内皮功能障碍、线粒体功能障碍以及妊娠期间高血压的产生。PE 中所见的慢性免疫激活会导致其他疾病的风险增加，例如心血管疾病、CKD、产后期间的痴呆以及随后妊娠期间的 PE。本综述的目的是强调表明不同淋巴细胞群在 PE 病理生理学中发挥作用的研究。此外，我们将讨论专注于恢复免疫平衡或针对特定免疫介体的治疗方法，这些方法可能是改善与 PE 相关的母婴结局的潜在策略。
