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<p>Female reproductive aging is linked to declining nicotinamide adenine dinucleotide (NAD<sup>+</sup>) levels and mitochondrial dysfunction. While nicotinamide mononucleotide (NMN) supplementation can counteract this, its mechanisms remain unclear. This study investigated NMN’s effects in aged female mice administered 200, 500, or 1000&#xa0;mg/kg/day NMN for 10 days, compared to aged and young controls. An optimal dose of 500&#xa0;mg/kg/day was identified for restoring ovarian follicle reserve. This treatment significantly increased ovarian NAD<sup>+</sup> and ATP, reduced oocyte oxidative stress (ROS) and apoptosis, and rejuvenated mitochondrial function. Mechanistically, NMN activated the NAD<sup>+</sup>/SIRT1/PGC-1α signaling pathway and upregulated the mitochondrial biogenesis protein TOMM20. In vitro, supplementing culture medium with 1 µM NMN optimally enhanced the developmental potential of aged oocytes. Both in vivo and in vitro interventions showed dose-dependent efficacy. We conclude that NMN mitigates ovarian aging by enhancing mitochondrial function via the NAD<sup>+</sup>/SIRT1/PGC-1α-TOMM20 axis.</p>

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NMN Can Restore Ovarian Reserve in Aged Mice by Upregulating NAD+/SIRT1/PGC-1α Signaling Pathway and TOMM20 Expression, and Improve in Vitro Development of Aging Oocytes

  • 期刊论文

  • 发表日期：

    2026年4月8日

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  • Jing Wang,
  • Qiqi Zhang,
  • Bo Yan,
  • Yongqi Fan,
  • Dandan Yang,
  • Ding Ding,
  • Chao Zhang,
  • Rufeng Xue,
  • Beili Chen,
  • Huijuan Zou,
  • Weiwei Zou,
  • Tinting Ye,
  • Qiushuang Wang,
  • Huiru Cheng,
  • Zhiguo Zhang,
  • Weihua Hu

摘要

Female reproductive aging is linked to declining nicotinamide adenine dinucleotide (NAD+) levels and mitochondrial dysfunction. While nicotinamide mononucleotide (NMN) supplementation can counteract this, its mechanisms remain unclear. This study investigated NMN’s effects in aged female mice administered 200, 500, or 1000 mg/kg/day NMN for 10 days, compared to aged and young controls. An optimal dose of 500 mg/kg/day was identified for restoring ovarian follicle reserve. This treatment significantly increased ovarian NAD+ and ATP, reduced oocyte oxidative stress (ROS) and apoptosis, and rejuvenated mitochondrial function. Mechanistically, NMN activated the NAD+/SIRT1/PGC-1α signaling pathway and upregulated the mitochondrial biogenesis protein TOMM20. In vitro, supplementing culture medium with 1 µM NMN optimally enhanced the developmental potential of aged oocytes. Both in vivo and in vitro interventions showed dose-dependent efficacy. We conclude that NMN mitigates ovarian aging by enhancing mitochondrial function via the NAD+/SIRT1/PGC-1α-TOMM20 axis.