Mitochondrial dysfunction is one of the hallmarks of aging. Consistently mitochondrial DNA (mtDNA) copy number and function decline with age in various tissues. There is increasing evidence to support that mitochondrial dysfunction drives ovarian aging. A decreased mtDNA copy number is also reported during ovarian aging. However, the mitochondrial mechanisms contributing to ovarian aging and infertility are not fully understood. Additionally, investigations into mitochondrial therapies to rejuvenate oocyte quality, select viable embryos and improve mitochondrial function may help enhance fertility or extend reproductive longevity in the future. These therapies include the use of mitochondrial replacement techniques, quantification of mtDNA copy number, and various pharmacologic and lifestyle measures. This review aims to describe the key evidence and current knowledge of the role of mitochondria in ovarian aging and identify the emerging potential options for therapy to extend reproductive longevity and improve fertility.

线粒体功能障碍是衰老的标志之一。在各种组织中，线粒体 DNA (mtDNA) 拷贝数和功能随着年龄的增长而持续下降。越来越多的证据支持线粒体功能障碍会导致卵巢衰老。在卵巢衰老过程中还报告了 mtDNA 拷贝数减少。然而，导致卵巢衰老和不孕的线粒体机制尚不完全清楚。此外，研究线粒体疗法以恢复卵母细胞质量、选择有活力的胚胎和改善线粒体功能可能有助于在未来提高生育能力或延长生殖寿命。这些疗法包括使用线粒体替代技术、mtDNA 拷贝数的量化以及各种药理学和生活方式措施。