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<p>Premature ovarian insufficiency (POI) is a common, heterogeneous disorder that affects up to 3.5% of women under 40 years of age and is defined by oligo/amenorrhoea, hypo-oestrogenism, and markedly elevated gonadotrophin levels. POI substantially increases risks for infertility, osteoporosis, cardiovascular disease, and psychological morbidity; however, its precise aetiology remains elusive, and current therapies rarely restore lasting ovarian function. This review synthesizes recent molecular, cellular, and animal data to clarify how six facets of mitochondrial dysregulation: oxidative stress, imbalanced dynamics (fusion/fission/mitophagy), defective biogenesis, altered mitochondrial DNA (copy-number and mutation), mitochondrial membrane potential, and disrupted electron-transport-chain activity—contribute to accelerated oocyte apoptosis, granulosa-cell dysfunction, and premature follicle loss. We further evaluate emerging mitochondria-targeted interventions, including small-molecule antioxidants, modulators of mitochondrial dynamics, biogenesis activators, autophagy regulators, mtDNA-protective agents, and innovative strategies such as mitochondrial transplantation. This article aims to systematically elaborate the mechanism of mitochondrial dysfunction in POI, summarize the treatment strategies for mitochondria, and provide a theoretical basis for clinical intervention.</p>

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Mechanisms and treatment modalities related to premature ovarian insufficiency in mitochondria: literature review

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年12月6日

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  • Huihui Li,
  • Xinyu Zhu,
  • Ruotong Ju,
  • Puhua Zhang,
  • Tingting Xue,
  • Shu Wang,
  • Ruixiang Zhu,
  • Jiali Luo,
  • Xuan Jing,
  • Xiangrong Cui

摘要

Premature ovarian insufficiency (POI) is a common, heterogeneous disorder that affects up to 3.5% of women under 40 years of age and is defined by oligo/amenorrhoea, hypo-oestrogenism, and markedly elevated gonadotrophin levels. POI substantially increases risks for infertility, osteoporosis, cardiovascular disease, and psychological morbidity; however, its precise aetiology remains elusive, and current therapies rarely restore lasting ovarian function. This review synthesizes recent molecular, cellular, and animal data to clarify how six facets of mitochondrial dysregulation: oxidative stress, imbalanced dynamics (fusion/fission/mitophagy), defective biogenesis, altered mitochondrial DNA (copy-number and mutation), mitochondrial membrane potential, and disrupted electron-transport-chain activity—contribute to accelerated oocyte apoptosis, granulosa-cell dysfunction, and premature follicle loss. We further evaluate emerging mitochondria-targeted interventions, including small-molecule antioxidants, modulators of mitochondrial dynamics, biogenesis activators, autophagy regulators, mtDNA-protective agents, and innovative strategies such as mitochondrial transplantation. This article aims to systematically elaborate the mechanism of mitochondrial dysfunction in POI, summarize the treatment strategies for mitochondria, and provide a theoretical basis for clinical intervention.