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素-14通过通过SLC7A11/GPX4抑制铁亡来缓解过早的卵巢衰竭

Rong Wu¹, Ting Wang¹, Xiaofeng Xu¹

¹Department of Obstetrics and Gynecology, The First Affiliated Hospital of Anhui Medical University, Hefei, China.

Drug development research

|June 24, 2025

概括

素-14 (PNX-14) 通过减少卵巢细胞中的氧化应激和铁亡,在治疗早产卵巢衰竭 (POF) 中表现有前途. 这种类疗法向ATF4/SLC7A11/GPX4通路,为POF提供了潜在的新疗法.

科学领域:

生殖生物学生殖生物学
细胞和分子医学是细胞和分子医学.
生物化学生化学

背景情况:

过早的卵巢衰竭 (POF) 具有早期卵巢衰退,卵泡储备减少和卵细胞质量受损的特征.
氧化应激和铁亡被确定为POF病变的关键贡献者.
素-14 (PNX-14) 和它的受体GPR173轴与卵巢功能有关.

研究的目的:

在早产卵巢衰竭 (POF) 的大鼠模型中研究Phoenixin-14 (PNX-14) 的治疗潜力.
阐明PNX-14在通过ATF4/SLC7A11/GPX4信号通路调节颗粒状细胞 (GC) 铁亡中的作用.

主要方法:

建立西斯普拉丁诱导的POF大鼠模型.
给予PNX-14并评估卵巢功能,氧化应激标志物 (MDA,SOD) 和铁亡指标.
分析血清PNX-14水平,GPR173表达和粒粉细胞中的分子信号通路 (ATF4,SLC7A11,GPX4).
将PNX-14与费罗斯塔丁-1 (Fer-1) 的疗效进行比较,并研究ATF4的淘汰效应.

主要成果:

被西斯普拉丁诱导的POF大鼠表现出下调的血清PNX-14和GPR173表达.
PNX-14治疗改善了卵巢重量,恢复了卵巢结构,并减少了氧化损伤 (减少MDA,增加SOD).
通过上调ATF4,SLC7A11和GPX4的调节,PNX-14抑制了GC铁亡,对亡的影响最小. 它的有效性与Fer-1相似.

结论:

素-14 (PNX-14) 在大鼠模型中有效缓解过早卵巢衰竭 (POF).
通过ATF4/SLC7A11/GPX4信号通路,PNX-14通过抑制粒粉细胞铁灭来发挥其保护作用.
PNX-14代表了对管理POF的有希望的治疗候选者.

关键词:

在GPX4中使用GPX4.在PNX-14.过早的卵巢衰竭是早期的卵巢衰竭.铁性化 (ferroptosis) 是一种

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