The article discusses the mechanisms of mitochondrial dysfunction in ovarian aging and potential interventions. Mitochondria play a crucial role in energy production and cellular functions, and their dysfunction is closely linked to ovarian aging. The study highlights that mitochondrial oxidative stress, mtDNA instability, and impaired mitochondrial quality control mechanisms contribute to ovarian aging. Oxidative stress, caused by an imbalance between reactive oxygen species (ROS) and antioxidants, leads to damage in oocytes and granulosa cells, affecting fertility. mtDNA copy number decreases with age, and mutations in mtDNA further impair mitochondrial function. Additionally, mitochondrial quality control mechanisms, such as biogenesis, dynamics, and autophagy, are disrupted in aging ovaries, leading to reduced mitochondrial function and oocyte quality. The article also explores potential interventions, including mitochondrial nutrition therapy, mitochondrial replacement therapy, and drugs targeting mitochondrial function. These interventions aim to improve mitochondrial health, reduce oxidative stress, and enhance oocyte quality. While some animal studies show promising results, more research is needed to validate these findings in humans and establish effective clinical treatments. The study emphasizes the importance of understanding mitochondrial mechanisms in ovarian aging to develop strategies for preserving fertility in aging women.The article discusses the mechanisms of mitochondrial dysfunction in ovarian aging and potential interventions. Mitochondria play a crucial role in energy production and cellular functions, and their dysfunction is closely linked to ovarian aging. The study highlights that mitochondrial oxidative stress, mtDNA instability, and impaired mitochondrial quality control mechanisms contribute to ovarian aging. Oxidative stress, caused by an imbalance between reactive oxygen species (ROS) and antioxidants, leads to damage in oocytes and granulosa cells, affecting fertility. mtDNA copy number decreases with age, and mutations in mtDNA further impair mitochondrial function. Additionally, mitochondrial quality control mechanisms, such as biogenesis, dynamics, and autophagy, are disrupted in aging ovaries, leading to reduced mitochondrial function and oocyte quality. The article also explores potential interventions, including mitochondrial nutrition therapy, mitochondrial replacement therapy, and drugs targeting mitochondrial function. These interventions aim to improve mitochondrial health, reduce oxidative stress, and enhance oocyte quality. While some animal studies show promising results, more research is needed to validate these findings in humans and establish effective clinical treatments. The study emphasizes the importance of understanding mitochondrial mechanisms in ovarian aging to develop strategies for preserving fertility in aging women.