晚期糖基化终末产物(AGEs)作为非酶糖基化反应的终末产物，其过量积累可通过氧化应激、炎症反应及细胞凋亡等机制参与多种眼部疾病的病理进程。文章系统综述了AGEs在糖尿病性角膜病变、白内障、青光眼、年龄相关性黄斑变性(ARMD)及糖尿病视网膜病变(DR)中的关键作用。研究发现，AGEs通过与受体RAGE结合，激活NADPH氧化酶、MAPK及NF-κB等信号通路，导致活性氧(ROS)生成、炎症因子释放及血管内皮功能紊乱，进而诱发角膜愈合延迟、晶状体蛋白交联、视神经退行性变、脉络膜新生血管(CNV)形成及血-视网膜屏障(BRB)破坏。例如，在糖尿病性角膜病变中，AGEs通过ROS/NLRP3炎性小体轴延缓伤口愈合； 在白内障中，抗坏血酸介导的AGEs导致的晶状体蛋白交联直接损害晶状体透明性； 在DR中，AGEs通过调控VEGF表达及周细胞凋亡加剧微血管损伤。此外，文章探讨了AGEs检测技术的进展与局限，如晶状体AGEscan荧光检测在糖尿病并发症筛查中的应用潜力，以及开发房水、玻璃体等组织特异性检测方法的必要性。针对治疗策略，提出抑制AGEs生成、阻断RAGE信号通路及开发抗糖基化药物的研究方向，强调其在延缓疾病进展中的临床价值。文章不仅整合了AGEs在眼病中的分子机制与临床关联，还为靶向干预提供了理论依据，对探索新型诊疗策略具有重要意义。

The excessive accumulation of advanced glycosylation end products(AGEs), the end products of non-enzymatic glycosylation reactions, can be involved in the pathological processes of various ocular diseases through mechanisms such as oxidative stress, inflammatory responses and apoptosis. In this paper, we systematically reviewed the key role of AGEs in diabetic keratopathy, cataract, glaucoma, age-related macular degeneration(ARMD)and diabetic retinopathy(DR). It was found that AGEs activate signalling pathways such as NADPH oxidase, MAPK and NF-κB by binding to the receptor RAGE, leading to reactive oxygen species(ROS)generation, release of inflammatory factors, and vascular endothelial dysfunction, which in turn induces delayed corneal healing, cross-linking of lens proteins, optic nerve degeneration, formation of choroidal neovascularisation(CNV), and blood-retinal barrier(BRB)disruption. For example, in diabetic keratopathy, AGEs delay wound healing via the ROS/NLRP3 inflammatory vesicle axis; in cataract, ascorbic acid-mediated cross-linking of lens proteins due to AGEs directly impairs lens transparency; and in DR, AGEs exacerbate microvascular damage by regulating vasucular endothelial growth factor(VEGF)expression and pericyte apoptosis. In addition, this article discusses the advances and limitations of AGEs detection techniques, such as the potential application of lens AGEscan fluorescence assay in screening for diabetic complications, and the need to develop tissue-specific assays for aqueous humour and vitreous. For therapeutic strategies, the research directions of inhibiting AGEs production, blocking RAGE signalling pathway and developing anti-glycosylation drugs are proposed to emphasise their clinical value in delaying disease progression. This review not only integrates the molecular mechanisms and clinical associations of AGEs in ocular diseases, but also provides a theoretical basis for targeted interventions, which is of great significance in exploring novel diagnostic and therapeutic strategies.

国家重点研发计划项目(No.2019YFC1710203); 山东省自然科学基金项目(No.ZR2021LZY045)