国际妇产科学杂志 ›› 2026, Vol. 53 ›› Issue (1): 89-92.doi: 10.12280/gjfckx.20251151

• 产科生理及产科疾病: 综述 • 上一篇    下一篇

Nrf2与子痫前期氧化应激的研究进展

任羽茜, 胡丽燕(), 任延旭   

  1. 030001 太原,山西医科大学(任羽茜);山西省儿童医院(胡丽燕);山西大同大学(任延旭)
  • 收稿日期:2025-10-14 出版日期:2026-02-15 发布日期:2026-03-11
  • 通讯作者: 胡丽燕 E-mail:15935136709@139.com

Research Progress on Nrf2 and Oxidative Stress in Preeclampsia

REN Yu-xi, HU Li-yan(), REN Yan-xu   

  1. Shanxi Medical University, Taiyuan 030001, China (REN Yu-xi); Shanxi Children's Hospital, Taiyuan 030032, China (HU Li-yan); Shanxi Datong University, Datong 037009, Shanxi Province, China (REN Yan-xu)
  • Received:2025-10-14 Published:2026-02-15 Online:2026-03-11
  • Contact: HU Li-yan E-mail:15935136709@139.com

摘要:

氧化应激是子痫前期关键的病理生理机制之一,因此,抗氧化应激对子痫前期及其相关并发症的防治具有重要的意义。本文系统综述了核转录因子红系2相关因子2(nuclear factor-erythroid 2-related factor 2,Nrf2)在子痫前期中调控氧化应激的分子机制及病理生理意义。近年研究发现,Nrf2与其负调控蛋白Kelch样ECH相关蛋白1(Kelch-like ECH-associated protein 1,KEAP1)构成的信号通路在子痫前期患者胎盘组织及动物模型中常呈表达失调或功能受损,导致下游抗氧化基因[如血红素加氧酶-1、NAD(P)H:醌氧化还原酶1]转录激活受抑制,加剧胎盘氧化损伤。进一步研究表明,Nrf2不仅调控抗氧化反应元件驱动的基因表达谱,还可通过影响血管内皮细胞功能及滋养细胞凋亡,参与胎盘形成与重塑。Nrf2是连接氧化应激与子痫前期病理进程的关键节点分子,其活化状态与疾病严重程度及进展密切相关。

关键词: 先兆子痫, 氧化性应激, 胎盘, 内皮细胞, 核转录因子红系2相关因子2

Abstract:

Oxidative stress is a key pathophysiological mechanism in preeclampsia. Therefore, antioxidant stress holds significant importance for the prevention and treatment of preeclampsia and its related complications. This paper systematically reviews the molecular mechanisms and pathophysiological significance of nuclear factor-erythroid 2-related factor 2 (Nrf2) in regulating oxidative stress in preeclampsia. Recent studies have found that the signaling pathway constituted by Nrf2 and its negative regulatory protein, Kelch-like ECH-associated protein 1 (KEAP1), is frequently dysregulated or functionally impaired in placental tissues of preeclampsia patients and in animal models. This impairment leads to the inhibited transcriptional activation of downstream antioxidant genes, such as heme oxygenase-1 and NAD(P)H:quinone oxidoreductase 1, thereby exacerbating placental oxidative damage. Further research indicates that Nrf2 not only regulates the gene expression profile driven by the antioxidant response element (ARE) but also participates in placental formation and remodeling by influencing vascular endothelial cell function and trophoblast apoptosis. Nrf2 is a key nodal molecule linking oxidative stress to the pathological progression of preeclampsia, and its activation status is closely associated with disease severity and progression.

Key words: Pre-eclampsia, Oxidative stress, Placenta, Endothelial cells, Nuclear factor-erythroid 2-related factor 2