[关键词]
[摘要]
神经血管单元(NVU)是由神经元、神经胶质细胞及微血管构成的复杂功能网络，其稳态失衡在青光眼发病机制中起关键作用。青光眼的发病机制可归结为视网膜神经节细胞-胶质细胞-微血管互动网络多重失衡。目前研究聚焦多靶点协同干预策略，通过重塑NVU整体稳态，为青光眼的神经保护提供新方向。文章综述了视网膜神经节细胞、胶质细胞及微血管的结构与功能改变，探讨了氧化应激与炎症、兴奋性毒性、神经-血管耦合失调、细胞通讯网络失衡及代谢废物清除障碍等多重机制的交互作用。
[Key word]
[Abstract]
The neurovascular unit(NVU)is a sophisticated functional network comprising neurons, glial cells, and microvessels. NVU's homeostatic imbalance plays a pivotal role in the pathogenesis of glaucoma. The disease mechanism can be attributed to disruptions within the interactive network among retinal ganglion cells, glial cells, and microvessels. Current research has increasingly focused on multi-target synergistic interventions aimed at restoring global NVU homeostasis. This provides novel avenues for neuroprotective strategies in glaucoma. This review summarizes the structural and functional alterations in these cellular components and discusses the interplay of multiple pathogenic mechanisms, including oxidative stress and inflammation, excitotoxicity, neurovascular uncoupling, dysregulation of intercellular communication, and impaired clearance of metabolic waste.
[中图分类号]
[基金项目]
四川省科技计划项目(No.2025ZNSFSC0570,2025ZNSFSC0574); 四川省中医药管理局科学技术研究专项课题项目(No.2023MS545); 四川省大学生创新创业训练计划省级立项(No.S202510633032); 成都市卫生健康委员会医学科研课题项目(No.2023029); 成都中医药大学“杏林学者”学科人才科研提升计划(No.CCYB2025001)
