国际生殖健康/计划生育杂志 ›› 2026, Vol. 45 ›› Issue (5): 395-400.doi: 10.12280/gjszjk.20260191

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烟酰胺腺嘌呤二核苷酸与卵巢功能障碍相关疾病的研究进展

李佳曼, 方颖, 杨晓葵,△()   

  1. 100026 北京, 首都医科大学附属北京妇产医院/北京妇幼保健院生殖医学科
  • 收稿日期:2026-04-10 出版日期:2026-09-15 发布日期:2026-09-20
  • 通讯作者: 杨晓葵,E-mail: yangxiaokui@ccmu.edu.cn
  • 作者简介:△审校者
  • 基金资助:
    国家自然科学基金面上项目(82271660);北京高层次创新创业人才支持计划(青年骨干人才项目)(G202531295);首都医科大学附属北京妇产医院“芒种计划”科技创新能力提升专项(FCYYMZA202502)

Research Advances of Nicotinamide Adenine Dinucleotide in Ovarian Dysfunction

LI Jia-man, FANG Ying, YANG Xiao-kui,△()   

  1. Department of Reproductive Medicine, Beijing Obstetrics and Gynecology Hospital, Capital Medical University, Beijing Maternal and Child Health Care Hospital, Beijing 100026, China
  • Received:2026-04-10 Published:2026-09-15 Online:2026-09-20
  • Contact: YANG Xiao-kui, E-mail: yangxiaokui@ccmu.edu.cn

摘要:

卵巢功能障碍相关疾病包括多囊卵巢综合征(polycystic ovary syndrome,PCOS)、早发性卵巢功能不全(premature ovarian insufficiency,POI)及卵巢储备功能减退(diminished ovarian reserve,DOR)等,是导致女性不孕和内分泌紊乱的重要病因,其发病机制涉及氧化应激失衡、线粒体功能障碍及代谢紊乱等多重病理环节。烟酰胺腺嘌呤二核苷酸(nicotinamide adenine dinucleotide,NAD+)作为参与细胞代谢与氧化还原调控的核心辅酶,其代谢失衡与卵巢病理进程密切相关。NAD+可通过影响胰岛素抵抗、卵巢炎症反应及氧化应激等参与PCOS的发生发展,并且可通过调控炎症反应、细胞焦亡及线粒体功能延缓卵巢功能减退。动物实验提示补充NAD+前体及抑制NAD+降解可改善卵巢功能,但其临床有效性及安全性仍需进一步验证。综述了NAD+的生物学特性、代谢途径及其在卵巢功能障碍相关疾病中的作用机制和相关干预策略的研究进展,旨在为卵巢功能障碍相关疾病的机制研究及临床诊疗提供新的理论依据和潜在治疗靶点。

关键词: NAD+, 多囊卵巢综合征, 原发性卵巢功能不全, 卵巢储备功能减退, 治疗

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