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精子干细胞中EGR1-Nudt16L1通路对丸缺血-再输液损伤的保护作用

Yiming Weng¹, Yanqiu Wang¹, Jun Xiang²

¹Department of Reproductive Center, Tongji Hospital, School of Medicine, Tongji University, Shanghai, China.

Cell biology international

|January 12, 2026

概括

转录因子EGR1通过激活Nudt16L1基因,保护精子干细胞免受丸损伤. 这一途径减少了氧化应激,并在缺血-再输液损伤后保持生育能力.

科学领域:

生殖生物学生殖生物学
细胞应激反应的应激反应
分子信号传输的方法

背景情况:

精子干细胞 (SSC) 对于精子生产至关重要,但易受丸缺血-再输液 (IR) 损伤的影响.
红外伤害会引起氧化应激,损害血液丸屏障 (BTB),并导致生殖细胞死亡.
转录因子EGR1促进SSC生存,但其体内保护机制尚不清楚.

研究的目的:

为了确定下游目标,调解EGR1对丸IR损伤的保护作用.
阐明EGR1保护SSCs的分子机制.

主要方法:

生物信息分析用于预测EGR1结合部位.
染色体免疫沉和光酶记者测定证实EGR1-Nudt16L1相互作用.
丸IR损伤的体内小鼠模型和体内SSC模型.

主要成果:

EGR1直接与Nudt16L1促进体结合,激活其表达.
过度表达EGR1减轻了IR诱导的丸损伤,改善了精子的运动性,并保持了BTB完整性.
沉默Nudt16L1取消了EGR1的保护作用;Nudt16L1的过度表达模仿了EGR1的保护.

结论:

Nudt16L1是EGR1的关键下游效应因子,可以保护SSC免受IR损伤.
EGR1-Nudt16L1轴通过减少氧化应激,维护BTB完整性和防止亡来对抗IR损伤.
这一途径代表了与丸扭曲和IR事件相关的不孕症的潜在治疗标.

关键词:

在 EGR1 里面,你会看到 EGR1 的位置.一个裸体的16L1 精子干细胞 (Spermatogonial stem cells) 是一种精子干细胞.灭症 (apoptosis) 是一种死亡的过程.血液试剂是屏障的障碍.缺血反注伤损伤氧化应激是一种氧化应激.

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