国际眼科纵览 ›› 2025, Vol. 49 ›› Issue (6): 422-431.doi: 10. 3760/cma.j.cn115500-20250822-25602

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神经炎症在青光眼视神经损害中的作用

谢骏青1  李谦1,2  张敬学1   

  1. 1 首都医科大学附属北京同仁医院 北京同仁眼科中心 北京市眼科研究所 视神经相关眼病智能诊断技术与设备研发北京市重点实验室,北京 100730; 2 河南省医学科学院,郑州 450000

  • 收稿日期:2025-08-22 出版日期:2025-12-22 发布日期:2025-12-22
  • 通讯作者: 张敬学,Email:jingxuezh@ccmu.edu.cn
  • 基金资助:
    国家自然科学基金(82130029);北京市属医学科研院所公益发展改革试点项目(JYY2023-6);中国博士后科学基金面上资助项目(2025M772091)

Neuroinflammation in glaucomatous optic neuropathy

Xie Junqing1, Li Qian1,2, Zhang Jingxue1   

  1. 1Beijing Institute of Ophthalmology, Beijing Tongren Eye Center, Beijing Tongren Hospital, Capital Medical University; Beijing Key Laboratory of Intelligent Diagnosis Technology and Equipment for Optic Nerve-Related Eye Diseases, Beijing 100730, China; 2Henan Academy of Innovations in Medical Science, Zhengzhou 450000, China
  • Received:2025-08-22 Online:2025-12-22 Published:2025-12-22
  • Contact: Zhang Jingxue, Email: jingxuezh@ccmu.edu.cn
  • Supported by:
    National Natural Science Foundation of China (82130029);Beijing Municipal Public Welfare Development and Reform Pilot Project for Medical Research Institutes (JYY2023-6);China Postdoctoral Science Foundation(2025M772091)

摘要: 青光眼是一组以视网膜神经节细胞进行性丢失和视神经损伤为病理特征的神经退行性疾病,其确切发病机制尚未完全阐明。近年研究显示,患者视网膜及视乳头部位星形胶质细胞与小胶质细胞显著活化,表现为细胞形态改变、迁移增生及损害亚型分子标志物的表达上调,同时患者血清中炎性因子水平显著升高,表明胶质活化及神经炎性反应在青光眼的病理生理过程中扮演重要角色。而调控星形胶质细胞或者小胶质细胞的健康稳态、抑制其产生的神经炎性反应,对视神经损害具有较好的保护作用。因此,深入探讨胶质细胞介导的神经炎性反应机制及其有潜能的调控策略,有望为青光眼视神经保护提供新的治疗靶点和干预方案。

关键词: 青光眼, 神经炎症, 星形胶质细胞, 小胶质细胞, 炎性因子

Abstract: Glaucoma represents a group of neurodegenerative disorders characterized by progressive loss of retinal ganglion cells and optic nerve injury, though its precise pathogenesis remains incompletely understood. Recent studies have revealed significant activation of astrocytes and microglia in the retina and optic nerve head of glaucoma patients, manifested by morphological changes, migration, proliferation, and upregulation of injury-related molecular markers. Concurrently, elevated levels of inflammatory factors are observed in patient serum, suggesting that glial activation and neuroinflammation play a critical role in the pathophysiology of glaucoma. Importantly, modulating the homeostasis of astrocytes or microglia and suppressing neuroinflammatory responses exert protective effects against optic nerve injury. Therefore, further investigation into the mechanisms of glia-mediated neuroinflammation and potential regulatory strategies may offer novel therapeutic targets and interventions for optic nerve protection in glaucoma.

Key words: Glaucoma, Neuroinflammation, Astrocyte, Microglia, Inflammatory factor