山东大学耳鼻喉眼学报 ›› 2024, Vol. 38 ›› Issue (2): 163-168.doi: 10.6040/j.issn.1673-3770.0.2023.333

• 综述 • 上一篇    

TLR4/NF-κB通道在糖尿病视网膜病变中的作用

伦英俊1,陈晨2,高宏程2,范清琳3,邰仁清1   

  1. 山东省医学科学院)研究生处, 山东 泰安 271000
  • 出版日期:2024-03-20 发布日期:2024-03-29
  • 通讯作者: 陈晨. E-mail:sdchenchen@126.com

Role of Toll-like receptor 4/nuclear transcription factor-κB channels in diabetic retinopathy

LUN Yingjun1, CHEN Chen2, GAO Hongcheng2, FAN Qinglin3, TAI Renqing1   

  1. 1. Department of Clinical Medical College, Weifang Medical College, Weifang 261000, Shandong, China2. Department of Ophthalmology, Linyi People's Hospital, Linyi 276000, Shandong, China3. Department of Postgraduate, Shandong First Medical University & Shandong Academy of Medical Sciences, Taian 271000, Shandong, China
  • Online:2024-03-20 Published:2024-03-29

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摘要： 糖尿病视网膜病变(diabetic retinopathy, DR)是一种由糖尿病引起的微血管并发症,也是导致患者失明的首要原因。其发病机制受多种因素影响,例如免疫炎症、氧化应激、多元醇途径等。目前认为免疫炎症机制在DR的发生发展起重要作用。Toll样受体4(Toll-like receptor 4, TLR4)/核转录因子-κB(nuclear factor kappa B, NF-κB)通路是介导炎症因子释放的重要途径,在免疫炎性机制中发挥关键作用。目前不少研究证实抑制TLR4/NF-κB信号通路可有效减轻DR。本文就TLR4/NF-κB通道在DR中的作用进行综述,可为治疗DR提供新的靶点。

关键词: 糖尿病视网膜病变, Toll样受体4, 核转录因子κB, 小胶质细胞, 炎症

Abstract: Diabetic retinopathy(DR)is a microvascular complication caused by diabetes mellitus and is the primary cause of blindness in patients. Its pathogenesis is influenced by various factors,such as immune inflammation, oxidative stress, and polyol pathways. Currently, immune-inflammatory responses are considered to play important roles in the development of DR. The Toll-like receptor 4(TLR4)/nuclear transcription factor-κB(NF-κB)pathway mediates the release of inflammatory factors and plays a key role in inflammatory mechanisms. Several studies have demonstrated that inhibition of the TLR4/NF-κB signaling pathway can effectively treat DR.This review addresses the role of TLR4/NF-κB channels in DR, which may provide novel treatment targets for this disease.

Key words: Diabetic retinopathy, Toll-like receptor 4, Nuclear factor kappa B, Microglia, Inflammation

中图分类号: 

  • R774.1
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