Scholarlink

<p>Premature ovarian insufficiency (POI) is a reproductive disorder lacking effective treatment options. This study explores the therapeutic potential of exosomes derived from human umbilical cord mesenchymal stem cells (HuMSCs-Exos) in restoring ovarian function in a cyclophosphamide (CTX)-induced POI mouse model. HuMSCs-Exos treatment significantly improved ovarian structure, restored follicular development, and normalized key hormone levels, enhancing estrous cycle regularity and fertility in POI mice. Mechanistic investigations revealed that HuMSCs-Exos promote SIRT3 expression, which modulates mitochondrial dynamics and reduces apoptosis in ovarian theca-interstitial cells (TICs). Furthermore, HuMSCs-Exos restored mitochondrial membrane potential and enhanced testosterone synthesis in TICs under CTX-induced stress, effects that were mitigated by the SIRT3 inhibitor 3-TYP, highlighting SIRT3 as a critical mediator. These findings indicate that HuMSCs-Exos support ovarian recovery, with effects consistent with the activation of SIRT3-mediated mitochondrial stabilization pathways in TICs, suggesting a promising therapeutic approach for POI.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

HuMSCs-derived exosomes alleviate premature ovarian insufficiency by enhancing SIRT3-mediated mitochondrial function in theca-interstitial cells

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年2月16日

查看全文
  • Xiangrong Cui,
  • Xinyu Zhu,
  • Jiali Luo,
  • Ruixiang Zhu,
  • Ruotong Ju,
  • Puhua Zhang,
  • Huihui Li,
  • Shu Wang,
  • Li Peng,
  • Chenyu Jia,
  • Tingting Xue,
  • Xuan Jing

摘要

Premature ovarian insufficiency (POI) is a reproductive disorder lacking effective treatment options. This study explores the therapeutic potential of exosomes derived from human umbilical cord mesenchymal stem cells (HuMSCs-Exos) in restoring ovarian function in a cyclophosphamide (CTX)-induced POI mouse model. HuMSCs-Exos treatment significantly improved ovarian structure, restored follicular development, and normalized key hormone levels, enhancing estrous cycle regularity and fertility in POI mice. Mechanistic investigations revealed that HuMSCs-Exos promote SIRT3 expression, which modulates mitochondrial dynamics and reduces apoptosis in ovarian theca-interstitial cells (TICs). Furthermore, HuMSCs-Exos restored mitochondrial membrane potential and enhanced testosterone synthesis in TICs under CTX-induced stress, effects that were mitigated by the SIRT3 inhibitor 3-TYP, highlighting SIRT3 as a critical mediator. These findings indicate that HuMSCs-Exos support ovarian recovery, with effects consistent with the activation of SIRT3-mediated mitochondrial stabilization pathways in TICs, suggesting a promising therapeutic approach for POI.