国际妇产科学杂志 ›› 2025, Vol. 52 ›› Issue (3): 241-245.doi: 10.12280/gjfckx.20241166

• 普通妇科疾病及相关研究: 综述 •    下一篇

子宫内膜异位症合并慢性子宫内膜炎的发病机制及其对生殖的影响

邵梦宇, 马赛花, 宫政, 赵晓丽, 赵志梅()   

  1. 300381 天津中医药大学第一附属医院生殖医学科,国家中医针灸临床医学研究中心
  • 收稿日期:2024-12-24 出版日期:2025-06-15 发布日期:2025-06-19
  • 通讯作者: 赵志梅 E-mail:zhaozhim2003@aliyun.com
  • 作者简介:审校者
  • 基金资助:
    国家自然科学基金(82205172)

Pathogenesis of Endometriosis Complicated with Chronic Endometritis and Its Impact on Reproduction

SHAO Meng-yu, MA Sai-hua, GONG Zheng, ZHAO Xiao-li, ZHAO Zhi-mei()   

  1. Department of Reproductive Medicine, First Teaching Hospital of Tianjin University of Traditional Chinese Medicine, National Clinical Research Center for Chinese Medicine Acupuncture and Moxibustion, Tianjin 300381, China
  • Received:2024-12-24 Published:2025-06-15 Online:2025-06-19
  • Contact: ZHAO Zhi-mei E-mail:zhaozhim2003@aliyun.com

摘要:

子宫内膜异位症(endometriosis,EMs)是育龄期女性常见的一种良性妇科疾病,越来越多的临床研究发现,EMs患者中慢性子宫内膜炎(chronic endometritis,CE)的发病风险增加,二者对女性生殖能力的负面影响也被广泛关注。EMs合并CE的潜在发病机制可能与免疫炎症状态、类固醇激素、微生物病原体、微小RNA相关。作为一种炎性疾病,EMs在发病过程中引起的免疫炎症变化直接促进了CE的发展。类固醇激素中的雌、孕激素浓度异常,尤其是雌激素升高,促进了EMs和CE共同发病。宫腔内外菌群的失衡通过局部免疫异常和炎症反应加速了EMs和CE共同发病的进程。作为基因表达的调控者,微小RNA通过影响各个通路蛋白的表达也在二者共同发病的过程中发挥作用。EMs和CE共同发病使得子宫内膜容受性进一步受损,影响女性生殖能力。综述EMs合并CE的发病机制及其对生殖的影响,以期为EMs的治疗提供新思路及依据。

关键词: 子宫内膜异位症, 子宫内膜炎, 生殖, 微RNAs, 免疫, 炎症, 慢性子宫内膜炎

Abstract:

Endometriosis (EMs) is a common benign gynecological disease among women of childbearing age. An increasing number of clinical studies have found that the risk of chronic endometritis (CE) is elevated in patients with EMs. The negative impacts of both conditions on female reproductive capacity have also drawn extensive attention. The potential pathogenesis of EMs complicated with CE may be related to immune-inflammatory state, steroid hormones, microbial pathogens, and microRNAs. As an inflammatory disease, the immune-inflammatory changes caused during the pathogenesis of EMs directly promote the development of CE. Abnormal concentrations of estrogen and progestogen in steroid hormones, especially elevated estrogen levels, contribute to the co-occurrence of EMs and CE. The imbalance of intra- and extra- uterine flora accelerates the co-pathogenesis of EMs and CE through local immune abnormalities and inflammatory responses. As regulators of gene expression, microRNAs also play a role in the co-morbidity process by influencing the expression of proteins in various pathways. The co-occurrence of EMs and CE further impairs endometrial receptivity and affects female reproductive capacity. This review summarizes the pathogenesis of EMs complicated with CE and its impact on reproduction, aiming to provide new ideas and evidence for the treatment of EMs.

Key words: Endometriosis, Endometritis, Reproduction, MicroRNAs, Immunity, Inflammation, Chronic endometritis