Mitochondrial dysfunction plays a critical role in ovarian aging, affecting oocyte quality and fertility. This review summarizes the mechanisms of mitochondrial dysfunction in ovarian aging and explores potential interventions. Mitochondria regulate cellular metabolism, proliferation, and apoptosis, and their dysfunction is linked to age-related pathologies. In ovarian aging, mitochondrial dysfunction leads to reduced mitochondrial DNA (mtDNA) copy number, impaired energy production, and increased oxidative stress (OS), which accelerate cellular senescence and oocyte aging. Mitochondrial damage is associated with telomere shortening, compromised autophagy, and loss of proteostasis, all contributing to ovarian aging. Additionally, mitochondrial dysfunction disrupts oocyte-cumulus cell communication, leading to reduced oocyte quality and fertility. Mitochondrial apoptosis pathways are also activated during ovarian aging, increasing cell apoptosis and follicular atresia. Telomere shortening, driven by OS and mitochondrial dysfunction, further exacerbates ovarian aging by impairing mitochondrial biosynthesis and DNA repair. Epigenetic regulation involving mitochondria also influences oocyte senescence. Potential interventions include mitochondrial nutrition therapy, such as antioxidants, coenzyme Q10, and NAD+ precursors, which improve mitochondrial function and reduce OS. Mitochondrial replacement therapy, including mitochondrial transplantation, aims to enhance oocyte quality by introducing healthy mitochondria. These interventions may help slow ovarian aging and improve fertility in women with advanced age. Further research is needed to validate these approaches in clinical settings.Mitochondrial dysfunction plays a critical role in ovarian aging, affecting oocyte quality and fertility. This review summarizes the mechanisms of mitochondrial dysfunction in ovarian aging and explores potential interventions. Mitochondria regulate cellular metabolism, proliferation, and apoptosis, and their dysfunction is linked to age-related pathologies. In ovarian aging, mitochondrial dysfunction leads to reduced mitochondrial DNA (mtDNA) copy number, impaired energy production, and increased oxidative stress (OS), which accelerate cellular senescence and oocyte aging. Mitochondrial damage is associated with telomere shortening, compromised autophagy, and loss of proteostasis, all contributing to ovarian aging. Additionally, mitochondrial dysfunction disrupts oocyte-cumulus cell communication, leading to reduced oocyte quality and fertility. Mitochondrial apoptosis pathways are also activated during ovarian aging, increasing cell apoptosis and follicular atresia. Telomere shortening, driven by OS and mitochondrial dysfunction, further exacerbates ovarian aging by impairing mitochondrial biosynthesis and DNA repair. Epigenetic regulation involving mitochondria also influences oocyte senescence. Potential interventions include mitochondrial nutrition therapy, such as antioxidants, coenzyme Q10, and NAD+ precursors, which improve mitochondrial function and reduce OS. Mitochondrial replacement therapy, including mitochondrial transplantation, aims to enhance oocyte quality by introducing healthy mitochondria. These interventions may help slow ovarian aging and improve fertility in women with advanced age. Further research is needed to validate these approaches in clinical settings.