在孕期糖尿病中,PGK1通过雌激醇-Keap1-Nrf2通路调节氧化应激
You Peng1, Hengli Zhao2, Jun Chen1
1Department of Obstetrics and Gynecology, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, China.
International journal of biological sciences
|September 17, 2025
概括
在孕期糖尿病 (GDM) 中,抑制糖酸激酶1 (PGK1) 降低了氧化应激. 这种方法通过雌激醇-Keap1-Nrf2通路恢复氧化还原平衡,为妊娠并发症提供潜在的治疗益处.
科学领域:
- 生殖生物学 生殖生物学
- 代谢障碍 代谢障碍 代谢障碍
- 细胞信号传输 细胞信号传输
背景情况:
- 孕期糖尿病 (GDM) 与显著的氧化应激 (OS) 有关.
- 糖酸酶1 (PGK1) 调节ATP的产生,其抑制激活了抗氧化途径.
- 此前,PGK1在GDM病原发生中的特定作用尚不清楚.
研究的目的:
- 研究PGK1在GDM相关的胎盘功能障碍中的作用.
- 探索PGK1抑制在GDM中的治疗潜力.
主要方法:
- 在人类GDM胎盘和小鼠模型中分析PGK1表达.
- 药物抑制和PGK1.1的lentivirus介导的淘汰.
- 对雌醇-Keap1-Nrf2信号通路的研究.
主要成果:
- 在GDM胎盘和模型中,PGK1被上调.
- 抑制PGK1改善了胎盘功能障碍,减少了活性氧物种 (ROS) 和改善了妊娠结果.
- 抑制PGK1提高了雌醇水平,促进了Keap1的二分化和Nrf2的激活.
结论:
- PGK1通过破坏氧化还原平衡,在GDM病变发生过程中发挥着至关重要的作用.
- 雌激醇-Keap1-Nrf2轴是PGK1影响GDM的关键机制.
- 对PGK1的药理抑制是治疗GDM相关并发症的一个有前途的治疗策略.
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