国际妇产科学杂志 ›› 2026, Vol. 53 ›› Issue (2): 137-142.doi: 10.12280/gjfckx.20251195

• 普通妇科疾病及相关研究: 综述 • 上一篇    下一篇

冷诱导RNA结合蛋白诱导阴道黏膜上皮损伤导致下生殖道感染的研究进展

其格乐, 乔峤()   

  1. 010030 呼和浩特内蒙古医科大学(其格乐); 内蒙古医科大学附属医院妇产科(乔峤)
  • 收稿日期:2025-10-23 出版日期:2026-04-15 发布日期:2026-05-08
  • 通讯作者: 乔峤 E-mail:qiaoqiao771011@126.com
  • 基金资助:
    内蒙古自治区医师协会项目(YSXH2024KYF027)

Research Progress in Cold-Inducible RNA-Binding Protein-Induced Vaginal Mucosal Epithelial Injury Leading to Lower Reproductive Tract Infection

QI Ge-le, QIAO Qiao()   

  1. Inner Mongolia Medical University, Hohhot 010030, China (QI Ge-le); Department of Obstetrics and Gynecology, The Affiliated Hospital of Inner Mongolia Medical University, Hohhot 010030, China (QIAO Qiao)
  • Received:2025-10-23 Published:2026-04-15 Online:2026-05-08
  • Contact: QIAO Qiao E-mail:qiaoqiao771011@126.com

摘要:

女性下生殖道感染是妇科常见疾病,其发病机制复杂,核心病理过程包括阴道黏膜上皮细胞损伤及屏障功能破坏。阴道黏膜上皮不仅是物理屏障,还参与局部免疫调控,其功能受炎症、微生物群及激素水平多重因素影响。冷诱导RNA结合蛋白(cold-inducible RNA-binding protein,CIRP)作为一种新型损伤相关分子模式(damage-associated molecular patterns,DAMPs),在多种黏膜组织炎症和屏障损伤中发挥关键作用。研究表明,CIRP可与Toll样受体4(Toll-like receptor 4,TLR4)及骨髓细胞触发受体1(triggering receptor expressed on myeloid cells-1,TREM-1)相互作用,激活核因子κB信号通路,诱导氧化应激、中性粒细胞胞外陷阱(neutrophil extracellular traps,NETs)形成及炎症,从而导致阴道黏膜上皮细胞凋亡和结构破坏。尽管CIRP在肠道、呼吸道等黏膜损伤中的作用已有明确证据,但其在阴道黏膜上皮损伤中的具体作用机制尚未阐明。结合现有文献推测,CIRP可能通过调控炎症信号转导、诱导上皮细胞凋亡及破坏细胞间连接等途径介导阴道黏膜上皮损伤,进而促进下生殖道感染的发生与复发。未来研究需聚焦于体外构建芯片类器官模型,检测CIRP与激素周期、局部免疫及阴道微生物群之间的相互作用,并探索基于CIRP调控的干预策略,以期为女性下生殖道感染的防治提供新思路。

关键词: 冷诱导RNA结合蛋白, RNA结合蛋白质类, 芯片类器官模型, 阴道黏膜屏障, 下生殖道感染, 中性粒细胞胞外陷阱

Abstract:

Lower reproductive tract infection in women is a common gynecological disorder with a complex pathogenesis. The core pathological processes include vaginal mucosal epithelial cell injury and disruption of barrier function. The vaginal mucosal epithelium serves not only as a physical barrier but also participates in local immune regulation, with its function being influenced by multiple factors such as inflammation, microbiota, and hormonal levels. Cold-inducible RNA-binding protein (CIRP), as a novel damage-associated molecular pattern (DAMP), plays a pivotal role in inflammation and barrier damage in various mucosal tissues. Studies have shown that CIRP can interact with Toll-like receptor 4 (TLR4) and triggering receptor expressed on myeloid cells-1 (TREM-1), activating the nuclear factor-κB signaling pathway, inducing oxidative stress, neutrophil extracellular traps (NETs) formation, and inflammation, ultimately leading to vaginal mucosal epithelial cell apoptosis and structural damage. Although the role of CIRP in mucosal injury in tissues such as the intestine and respiratory tract is well-established, its specific mechanism in vaginal mucosal epithelial injury remains to be elucidated. Based on existing literature, it is hypothesized that CIRP may mediate vaginal mucosal epithelial damage by regulating inflammatory signal transduction, inducing epithelial cell apoptosis, and disrupting intercellular junctions, thereby promoting the occurrence and recurrence of lower reproductive tract infection. Future research should focus on constructing in vitro organ-on-a-chip models to examine the interactions among CIRP, the hormonal cycle, local immunity, and vaginal microbiota, and explore intervention strategies based on CIRP regulation, with the aim of providing new insights for the prevention and treatment of female lower reproductive tract infection.

Key words: Cold-inducible RNA-binding protein, RNA-binding proteins, Organ-on-a-chip model, Vaginal mucosal barrier, Lower reproductive tract infection, Neutrophil extracellular traps