NRF2-TERT-ACSL4通路抑制铁和调节细胞骨动力学,以缓解卵巢衰老
Yaxin Chen1, Jing Zhang2, Shuangshuang Cui1
1Department of Obstetrics and Gynecology, NHC Key Laboratory of Study on Abnormal Gametes and Reproductive Tract, the First Affiliated Hospital of Anhui Medical University, Hefei, 230022, Anhui, China; Engineering Research Center of Biopreservation and Artificial Organs, Ministry of Education, Hefei, 230032, Anhui, China; Anhui Province Key Laboratory of Reproductive Disorders and Obstetrics and Gynecology Diseases, Hefei, 230032, Anhui, China.
International journal of biological macromolecules
|March 11, 2026
概括
静态磁场通过激活NRF2/TERT/ACSL4通路来保护卵巢老化. 这种干预通过减少铁亡和恢复细胞骨组织来保护卵巢功能.
科学领域:
- 生殖生物学 生殖生物学
- 细胞衰老 细胞衰老
- 生物物理学的生物物理.
背景情况:
- 卵巢衰老导致生殖能力下降,与氧化应激,铁亡以及细胞骨问题有关.
- 铁亡的分子机制和对卵巢衰老的治疗干预措施尚未完全理解.
研究的目的:
- 调查NRF2/TERT/ACSL4轴在与卵巢衰老相关的铁和细胞骨变化的研究.
- 探索静态磁场 (SMF) 作为一种非药物学方法来激活NRF2信号和减轻卵巢衰老.
主要方法:
- 利用自然衰老的小鼠和D-银糖诱导的衰老细胞.
- 采用了组织学,生物化学,线粒体和分子分析.
- 使用NRF2调节剂 (ML385,SFN) 和端粒酶抑制剂 (BIBR1532) 的验证结果.
主要成果:
- SMF激活了NRF2/TERT/ACSL4轴,减少了卵巢衰老和铁亡.
- SMF维持了铁的稳态,并恢复了F-actin细胞骨组织.
- NRF2直接上调TERT表达;p62酸化促进了NRF2激活,由SMF触发.
结论:
- 激活NRF2/TERT/ACSL4通路对于防止卵巢衰老至关重要.
- 这条通路协调铁灭抑制和细胞骨重塑.
- 在老化过程中,SMF暴露提供了一种潜在的生物物理策略,以保持卵巢功能.
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