纤维细胞生长因子19通过FGFR4-ERK-NRF2通路调节多囊卵巢综合征的进展
Junjie Qu1, Meiting Qiu1, Jingyun Wang1
1Department of Reproductive Medicine, Shanghai First Maternity and Infant Hospital, Tongji University School of Medicine, Shanghai, China.
Frontiers in cell and developmental biology
|September 15, 2025
概括
纤维细胞生长因子19 (FGF19) 可能通过影响FGFR4-ERK-NRF2通路在多囊卵巢综合征 (PCOS) 中发挥作用. 这项研究发现PCOS患者的FGF19水平升高,并探索了其分子机制.
科学领域:
- 内分泌学 在内分泌学.
- 分子生物学分子生物学
- 生殖医学 生殖医学
背景情况:
- 纤维细胞生长因子19 (FGF19) 是一种内分泌激素,对卵巢功能至关重要.
- 多囊卵巢综合征 (PCOS) 是一种复杂的内分泌疾病,具有显著的生殖和代谢影响.
- 在PCOS中FGF19的作用背后的特定分子机制仍然不完全理解.
研究的目的:
- 调查FGF19在PCOS病变发生过程中的作用.
- 阐明涉及PCOS中FGFR4-ERK-NRF2通路的分子机制.
- 评估FGF19在氧化应激条件下对卵巢细胞的影响.
主要方法:
- 来自PCOS患者和对照组的毛囊液的蛋白质组分析.
- 建立一个PCOS小鼠模型用于机制研究.
- 在体外实验中使用KGN细胞来评估FGF19在有或没有氧化应激 (H2O2) 的影响.
主要成果:
- 蛋白质组学揭示了PCOS中差异性蛋白质表达,与VEGF和氧化酸化等途径有关.
- 在PCOS患者和小鼠中,FGF19/FGF15水平升高.
- 在KGN细胞中FGF19的过度表达促进了活力和抑制了亡,调节了FGFR4-ERK-NRF2通路;这些效应被FGFR4抗剂逆转.
- 在KGN细胞中,FGF19抵消了H2O2诱导的氧化应激,提高了活力,降低了亡和ROS水平.
结论:
- FGF19与PCOS的发展和进展有关.
- FGFR4-ERK-NRF2通路是FGF19在PCOS中发挥作用的关键分子机制.
- FGF19在卵巢细胞中表现出对氧化应激的保护作用,这表明其具有治疗潜力.
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