国际生殖健康/计划生育杂志 ›› 2026, Vol. 45 ›› Issue (2): 145-149.doi: 10.12280/gjszjk.20250636

• 综述 • 上一篇    下一篇

高龄卵母细胞质量衰退的免疫学机制

魏元杰, 苑丽华, 孙振高()   

  1. 250014 济南,山东中医药大学第一临床医学院(魏元杰,苑丽华);山东中医药大学附属医院生殖与遗传科(孙振高)
  • 收稿日期:2025-12-24 出版日期:2026-03-15 发布日期:2026-04-07
  • 通讯作者: 孙振高 E-mail:sunzhengao77@126.com
  • 基金资助:
    国家重点研发计划项目(2024YFC3505800);国家自然科学基金面上项目(82474561)

Immunological Mechanism of Quality Decline in Elderly Oocytes

WEI Yuan-jie, YUAN Li-hua, SUN Zhen-gao()   

  1. The First Clinical College, Shandong University of Chinese Medicine, Jinan 250014, China (WEI Yuan-jie, YUAN Li-hua);Department of Reproduction and Genetics, The Affiliated Hospital of Shandong University of Chinese Medicine, Jinan 250014, China (SUN Zhen-gao)
  • Received:2025-12-24 Published:2026-03-15 Online:2026-04-07
  • Contact: SUN Zhen-gao E-mail:sunzhengao77@126.com

摘要:

卵母细胞衰老是高龄女性生育力下降的核心环节。研究发现,高龄卵母细胞质量衰退与卵巢免疫微环境紊乱相关。巨噬细胞及T淋巴细胞等免疫细胞比例失衡,打破免疫稳态并驱动卵巢纤维化;炎性因子与炎症小体过度表达直接破坏卵母细胞纺锤体结构,干扰减数分裂进程;衰老相关分泌表型(senescence-associated secretory phenotype,SASP)介导的局部慢性炎症破坏卵巢局部免疫稳态;线粒体功能异常导致免疫轴功能紊乱以及铁死亡激活卵巢免疫衰老等协同调控作用有着密切的联系。通过破坏卵母细胞骨架、降低减数分裂能力、加剧氧化应激以及诱导细胞凋亡等途径,这些紊乱直接或间接导致卵母细胞质量下降及胚胎发育潜能受损。从免疫学角度综述高龄相关的卵母细胞质量衰退的作用机制,为后续开发靶向卵巢免疫微环境的生育力改善策略提供参考。

关键词: 卵母细胞, 衰老, 免疫, 衰老相关分泌表型, 铁死亡

Abstract:

Oocyte senescence is the core link of fertility decline in older women. Studies have found that the decline of oocyte quality is related to the disturbance of ovarian immune microenvironment in ageing women. Imbalanced proportions of immune cells such as macrophages and T lymphocytes disrupts the immune homeostasis and drives ovarian fibrosis. The overexpression of inflammatory factors and inflammasomes directly destroys the spindle structure of oocytes and interferes with meiosis. The local chronic inflammation mediated by senescence-associated secretory phenotype (SASP) disrupts the local immune homeostasis of ovary. Mitochondrial dysfunction leads to dysfunction of immune axis, and ferroptosis activates a new type of ovarian immunosenescence, which is closely related to the synergistic regulatory effects. By destroying the oocyte skeleton, reducing meiosis ability, exacerbating oxidative stress and inducing apoptosis, these disorders directly or indirectly lead to the decline of oocyte quality and the impairment of embryonic development potential. This paper reviews the mechanisms of age-related oocyte quality decline from the perspective of immunology, and provides a reference for the subsequent development of fertility improvement strategies targeting the ovarian immune microenvironment.

Key words: Oocytes, Aging, Immunity, Senescence-associated secretion phenotype, Ferroptosis