Abstract:

Ovarian dysfunction disorders, including polycystic ovary syndrome (PCOS), premature ovarian insufficiency (POI) and diminished ovarian reserve (DOR), are important causes of female infertility and endocrine disorders. Their pathogenesis involves multiple pathological processes, including oxidative stress imbalance, mitochondrial dysfunction, and metabolic disturbances. Nicotinamide adenine dinucleotide (NAD⁺), a central coenzyme involved in cellular metabolism and redox regulation, has been increasingly recognized as a factor closely associated with ovarian physiology and pathology. The abnormal expression of NAD⁺ participates in the pathogenesis of PCOS by modulating insulin resistance, ovarian inflammation, and oxidative stress. In addition, NAD⁺ may delay the ovarian functional decline through the regulation of inflammatory responses, pyroptosis, and mitochondrial function. Evidence from animal studies suggests that supplementation with NAD⁺ precursors or inhibition of NAD⁺ degradation, can improve ovarian function. However, the clinical efficacy and safety of these interventions remain to be further validated. This review summarizes the biological characteristics and metabolic pathways of NAD⁺, as well as its mechanisms of action and therapeutic strategies in ovarian dysfunction disorders, so as to provide new insights into the pathogenesis of ovarian dysfunction and to identify potential therapeutic targets for their clinical management.

Key words: NAD⁺, Polycystic ovary syndrome, Primary ovarian insufficiency, Diminished ovarian reserve, Therapy