O-001 Human Reproduction Keynote lecture: Human ovarian aging is characterized by oxidative damage and mitochondrial dysfunction

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Abstract The remarkable success of IVF has brought hope to millions worldwide. However, the age-related decline in female fertility due to diminishing oocyte quality remains a central challenge that current ART cannot fully overcome. Understanding the underlying cellular mechanisms is key to developing effective strategies for women of advanced maternal age. Evidence demonstrates that human ovarian aging is intrinsically linked to accumulating oxidative damage and progressive mitochondrial dysfunction within the oocyte, processes initiated surprisingly early in follicular development. Age-dependent increases in oxidative stress markers and significant metabolic perturbations—including NAD+ depletion and altered redox balance—are indicative of mitochondrial inefficiency in human oocytes. These insights provide a mechanistic basis for age-related subfertility and suggest potential therapeutic targets. Hypothetical interventions aimed at mitigating this decline include targeted nutritional support or optimized gamete and embryo culture media designed to bolster oocyte and embryo mitochondrial health. Furthermore, the promise of artificial intelligence to accelerate the discovery of novel compounds for such targeted interventions is rapidly unfolding, bringing excitement, but also a clear need for responsible implementation. Translating these possibilities into safe and effective clinical practice requires stringent validation. There is an urgent need for robust translational pipelines—incorporating rigorous pre-clinical and clinical testing, long-term safety follow-up, and adaptive regulatory oversight—to ensure responsible innovation as we seek to improve fertility outcomes for women of advanced maternal age.

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