诊断学理论与实践

诊断学理论与实践 ›› 2025, Vol. 24 ›› Issue (01): 80-88.doi: 10.16150/j.1671-2870.2025.01.012

• 综述 • 上一篇    下一篇

胰高血糖素样肽1受体激动剂在糖尿病视网膜病变中的作用机制研究进展

何翠环1, 石德荣1, 孙丹丹1, 李育蕊1, 夏广昊2()   

  1. 1.甘肃中医药大学第一临床医学院 甘肃 兰州 730000
    2.甘肃省人民医院内分泌科 甘肃 兰州 730000
  • 收稿日期:2025-01-24 接受日期:2025-02-08 出版日期:2025-02-25 发布日期:2025-02-25
  • 通讯作者: 夏广昊 E-mail：285743685@qq.com
  • 基金资助:
    甘肃省科技计划项目(20JR10RA397)

Research progress on mechanisms of glucagon-like peptide-1 receptor agonists in diabetic retinopathy

HE Cuihuan1, SHI Derong1, SUN Dandan1, LI Yurui1, XIA Guanghao2()   

  1. 1. First Clinical Medical Department, Gansu University of Chinese Medicine, Lanzhou 730000, Gansu Province, China
    2. Department of Endocrinology, Gansu Provincial Hospital, Lanzhou 730000, Gansu Province, China
  • Received:2025-01-24 Accepted:2025-02-08 Published:2025-02-25 Online:2025-02-25

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摘要：

糖尿病的患病率在我国甚至全球都呈逐年递增趋势，糖尿病视网膜病变（diabetic retinopathy， DR）的患者数量也随之增加，糖尿病的全球患病率约为34.6%，其中约30%的患者会发展为DR，而DR可导致失明，是成年人眼睛失明的主要原因。我国糖尿病患者的DR患病率为16.3%，城乡差异不显著，1型糖尿病患者的DR患病率为40.6%，2型糖尿病患者的DR患病率为37.3%。DR的发生涉及多种相互交叉作用的机制，包括炎症反应、小胶质细胞活化、氧化应激、晚期糖基化终末产物（advanced glycation end-products， AGE）蓄积、血管内皮生长因子（vascular endothelial growth factor， VEGF）增加、视网膜神经变性、血-视网膜屏障（blood-retina barrier， BRB）损伤等，但其发生机制尚未完全明确，目前临床治疗手段并不能完全阻止DR的进展及视力丧失。在胰高血糖素样肽1受体激动剂（glucagon-like peptide-1 receptor agonists， GLP-1RA）的相关研究中发现，GLP-1RA可通过多方面的分子机制和细胞通路对DR产生保护作用，如抑制胶质细胞活化、抑制炎症因子释放、抑制核因子κB（nuclear factor κB， NF-κB）信号通路、减少活性氧（reactive oxygen species， ROS）的产生和AGE沉积、线粒体保护、血管内皮细胞保护、神经保护及代谢调控等，可减缓或控制DR的发生、发展。本文从抗炎、抗氧化应激及抗新生血管形成，综述GLP-1RA在缓解或控制DR发生、发展中的作用机制进展，为后期DR的治疗选择提供理论参考。

关键词: 糖尿病视网膜病变, 胰高血糖素样肽1受体激动剂, 抗炎, 抗氧化应激, 抗新生血管形成

Abstract:

The prevalence of diabetes mellitus (DM) and its complication, diabetic retinopathy (DR), continues to rise year by year in China and globally. The global prevalence of DM is approximately 34.6%, with around 30% of patients progressing to DR, which is a major cause of adult blindness. In China, the DR prevalence among DM patients is 16.3%, with no significant urban-rural disparity. Notably, patients with type 1 diabetes mellitus (T1DM) and type 2 diabetes mellitus (T2DM) show substantially higher DR prevalence rates of 40.6% and 37.3%, respectively. The pathogenesis of DR involves complex interplay among multiple mechanisms, including inflammatory responses, microglial activation, oxidative stress, accumulation of advanced glycation end-products (AGEs), vascular endothelial growth factor (VEGF) upregulation, retinal neurodegeneration, and blood-retinal barrier (BRB) disruption. However, the precise mechanisms remain incompletely understood, and current clinical interventions cannot fully halt DR progression or prevent irreversible vision loss. Recent studies on glucagon-like peptide-1 receptor agonists (GLP-1RAs) demonstrate their protective effects against DR through multifaceted molecular mechanisms and cellular pathways. These include suppressing glial cell activation, inhibi-ting the release of inflammatory factors, blocking the nuclear factor κB (NF-κB) signaling pathway, and reducing reactive oxygen species (ROS) generation, along with AGE deposition, mitochondrial protection, vascular endothelial cell protection, neuroprotection, and metabolic regulation. Consequently, GLP-1RAs can mitigate or control the onset and progression of DR. This review summarizes the mechanisms by which GLP-1RAs alleviate or control the onset and progression of DR through anti-inflammatory, antioxidative stress, and anti-angiogenic effects, providing a theoretical reference for future DR treatment strategies.

Key words: Diabetic retinopathy, Glucagon-like peptide-1 receptor agonists, Anti-inflammation, Antioxidative stress, Inhibit neovascularization

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