Lin Bin, Li Dongkan
Xiamen Eye Center and Eye Institute of Xiamen University, School of Medicine, Xiamen, China.
Clinical Research Center for Eye Diseases, Xiamen, Fujian, China.
Front Immunol. 2025 May 23;16:1577200. doi: 10.3389/fimmu.2025.1577200. eCollection 2025.
Glaucoma, a leading cause of irreversible vision loss, is becoming more prevalent with the aging population, burdening patients, families, and society. In the past, the role of inflammatory factors in its pathogenesis was overlooked. This systematic review, based on a PubMed search and strict screening of 61 articles, selected 19 for in-depth analysis. It was found that multiple inflammatory factors like Tumor Necrosis factor alpha (TNF - α), Interleukin-6 (IL-6), and Interleukin-1 (IL-1) are abnormal in glaucoma patients' intraocular fluid. They impact trabecular meshwork function, damage retinal ganglion cells, and activate the complement system. Other factors such as Vascular Endothelial Growth Factor (VEGF) and Monocyte Chemoattractant Protein-1 (MCP-1) also contribute to the disease process. Based on these findings, emerging therapeutic strategies for glaucoma may include biological agents targeting specific inflammatory mediators, multitarget anti-inflammatory approaches, and personalized interventions guided by inflammatory biomarker profiling. However, critical challenges such as blood-retinal barrier penetration limitations, systemic immunosuppression risks, and technical hurdles in gene therapy delivery require further investigation. This systematic review synthesizes current evidence to inform clinical decision-making regarding inflammatory biomarker monitoring while identifying key knowledge gaps in ocular immunomodulation. The findings underscore the necessity for translational studies bridging preclinical models with clinical applications, ultimately aiming to optimize therapeutic outcomes for glaucoma patients worldwide.
青光眼是不可逆视力丧失的主要原因，随着人口老龄化，其发病率越来越高，给患者、家庭和社会带来沉重负担。过去，炎症因子在其发病机制中的作用被忽视了。本系统评价基于PubMed检索并严格筛选61篇文章，选取19篇进行深入分析。研究发现，青光眼患者眼内液中多种炎症因子如肿瘤坏死因子α（TNF-α）、白细胞介素-6（IL-6）和白细胞介素-1（IL-1）异常。它们影响小梁网功能，损害视网膜神经节细胞，并激活补体系统。其他因子如血管内皮生长因子（VEGF）和单核细胞趋化蛋白-1（MCP-1）也参与疾病过程。基于这些发现，青光眼新出现的治疗策略可能包括针对特定炎症介质的生物制剂、多靶点抗炎方法以及由炎症生物标志物谱指导的个性化干预。然而，诸如血视网膜屏障穿透限制、全身免疫抑制风险以及基因治疗递送中的技术障碍等关键挑战需要进一步研究。本系统评价综合了当前证据，为炎症生物标志物监测的临床决策提供信息，同时确定眼部免疫调节中的关键知识空白。研究结果强调了开展将临床前模型与临床应用相联系的转化研究的必要性，最终目标是优化全球青光眼患者的治疗效果。
