国际妇产科学杂志 ›› 2025, Vol. 52 ›› Issue (4): 451-456.doi: 10.12280/gjfckx.20250213

• 普通妇科疾病及相关研究:综述 • 上一篇    下一篇

慢性子宫内膜炎对子宫内膜容受性的影响机制研究进展

苏涵, 郭洁(), 宋殿荣, 张崴   

  1. 301617 天津中医药大学研究生院(苏涵);天津中医药大学第二附属医院妇产科(郭洁,宋殿荣,张崴)
  • 收稿日期:2025-03-04 出版日期:2025-08-15 发布日期:2025-09-08
  • 通讯作者: 郭洁,E-mail:guojie76@126.com
  • 作者简介:审校者
  • 基金资助:
    天津市教委科研计划重点项目(2021ZD027)

Research Progress on the Mechanism of the Effect of Chronic Endometritis on Endometrial Receptivity

SU Han, GUO Jie(), SONG Dian-rong, ZHANG Wei   

  1. Graduate School of Tianjin University of Traditional Chinese Medicine, Tianjin 301617, China (SU Han); Department of Obstetrics and Gynecology, The Second Affiliated Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin 300250, China (GUO Jie, SONG Dian-rong, ZHANG Wei)
  • Received:2025-03-04 Published:2025-08-15 Online:2025-09-08
  • Contact: GUO Jie, E-mail: guojie76@126.com

摘要:

慢性子宫内膜炎(chronic endometritis,CE)是一种以子宫内膜间质水肿、充血、不规则增厚及子宫内膜间质中存在浆细胞浸润为特征的炎症性疾病。近年研究表明,CE可通过多重机制降低子宫内膜容受性,导致不孕、反复种植失败及复发性流产等不良妊娠结局。具体机制包括:子宫内膜免疫细胞比例失衡引发的宫腔免疫微环境紊乱;乳杆菌属丰度降低伴随条件致病菌丰度增多所致的宫腔微生物稳态破坏;雌激素受体表达升高及孕激素反应性降低导致的激素调控网络失调;缺氧诱导因子、血管内皮生长因子等促血管生成因子过度表达引发的子宫内膜血管生成异常。深入阐释上述机制与子宫内膜容受性的关系,有助于为CE的临床精准诊断、靶向治疗及改善生育结局提供理论依据,对保障女性生殖健康具有重要意义。

关键词: 子宫内膜炎, 妊娠结局, 胚胎植入, 慢性子宫内膜炎, 子宫内膜容受性

Abstract:

Chronic endometritis (CE) is an inflammatory disease characterized by endometrial stromal edema, hyperemia, irregular thickening, and the presence of plasma cell infiltration. Recent studies have demonstrated that CE can reduce endometrial receptivity through multiple mechanisms, leading to adverse pregnancy outcomes such as infertility, recurrent implantation failure, and recurrent miscarriage. The specific mechanisms include: the disorder of the intrauterine immune microenvironment caused by the imbalance of the proportions of endometrial immune cells; the disruption of the intrauterine microbial homeostasis due to the decrease in the abundance of Lactobacillus and the increase of conditional pathogens; the dysregulation of the hormonal regulatory network resulting from the increased expression of estrogen receptors and the decreased responsiveness to progesterone; and the abnormal angiogenesis of the endometrium triggered by the overexpression of pro-angiogenic factors such as hypoxia-inducible factor and vascular endothelial growth factor. Elucidating the relationships between the above mentioned mechanisms and endometrial receptivity could provide a theoretical basis for the accurate clinical diagnosis, targeted therapies of CE, and the improvement of reproductive outcomes, and is of great significance for safeguarding female reproductive health.

Key words: Endometritis, Pregnancy outcome, Embryo implantation, Chronic endometritis, Endometrial receptivity