国际生殖健康/计划生育杂志 ›› 2026, Vol. 45 ›› Issue (3): 230-235.doi: 10.12280/gjszjk.20260032

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驱动蛋白家族成员18B在女性生殖功能中作用机制的研究进展

王薇(), 戴柏, 沙日娜, 托娅()   

  1. 010050 呼和浩特, 内蒙古医科大学(王薇)内蒙古医科大学附属医院生殖医学中心(戴柏,托娅),病理科(沙日娜)
  • 收稿日期:2026-01-23 出版日期:2026-05-15 发布日期:2026-06-02
  • 通讯作者: 托娅,E-mail:nmgty81@163.com
  • 作者简介:审校者

Research Progress on the Mechanism of KIF18B in Female Reproductive Function

WANG Wei(), DAI Bai, SHA Ri-na, TUO Ya()   

  1. Inner Mongolia Medical University, Hohhot 010050, China (WANG Wei); Center for Reproductive Medicine (DAI Bai, TUO Ya), Department of Pathology (SHA Ri-na), Affiliated Hospital of Inner Mongolia Medical University, Hohhot 010050, China
  • Received:2026-01-23 Published:2026-05-15 Online:2026-06-02
  • Contact: TUO Ya, E-mail: nmgty81@163.com

摘要:

女性生育力的维持与衰退是一个复杂的生理过程。驱动蛋白家族成员18B(kinesin family member 18B,KIF18B)通过调控纺锤体微管动力学确保染色体的精准排列与分离,从而维持基因组稳定性。基于其在细胞分裂中的关键功能,KIF18B在女性生殖系统中的潜在作用逐渐受到关注。KIF18B可能通过影响减数分裂纺锤体组装参与卵母细胞成熟,其与磷脂酰肌醇3激酶/蛋白激酶B/哺乳动物雷帕霉素靶蛋白复合物1(phosphoinositide 3-kinase/protein kinase B/mechanistic target of rapamycin complex 1,PI3K/Akt/mTORC1)等信号通路的关联提示其在原始卵泡激活及卵巢衰老进程中发挥潜在作用。此外,KIF18B对微管动力学的调节提示其参与子宫内膜结构重塑,并作为Wnt/β-联蛋白(β-catenin)通路的上游调控节点影响容受性建立。KIF18B功能障碍与卵子非整倍体率升高、卵巢储备功能下降及子宫内膜容受性降低之间的关系会进一步增加不良妊娠结局发生风险。综述KIF18B的分子机制与功能,阐述其在生殖关键过程的调控作用及其功能障碍与不良妊娠结局的潜在关联,并展望其作为生育功能评估标志物的价值。

关键词: 细胞分裂, 非整倍性, 胚胎植入, 妊娠结局, 驱动蛋白家族成员18B

Abstract:

The maintenance and decline of female fertility is a complex physiological process. Kinesin family member 18B (KIF18B) maintains the genome stability by regulating spindle microtubule dynamics to ensure the accurate alignment and segregation of chromosomes. Given the critical role of KIF18B in cell division, its potential functions in the female reproductive system have also attracted attention. KIF18B may participate in oocyte maturation by affecting meiotic spindle assembly, and its association with signaling pathways such as phosphoinositide 3-kinase/protein kinase B/mechanistic target of rapamycin complex 1 (PI3K/Akt/mTORC1) suggests a potential role in primordial follicle activation and ovarian aging. In addition, the regulation of KIF18B on microtubule dynamics implies the involvement in endometrial structural remodeling. As an upstream regulatory node of the Wnt/β-catenin pathway, KIF18B influences the establishment of endometrial receptivity. Dysfunction of KIF18B, including the increased rate of oocyte aneuploidy, the diminished ovarian reserve, and the reduced endometrial receptivity could further increase the risk of adverse pregnancy outcomes. This review summarizes the molecular mechanisms and functions of KIF18B, elucidates its regulatory roles in key reproductive processes and the potential links between its dysfunction and poor pregnancy outcomes, and discusses its prospective value as a biomarker for assessing fertility.

Key words: Cell division, Aneuploidy, Embryo implantation, Pregnancy outcome, Kinesin family member 18B