国际眼科纵览 ›› 2026, Vol. 50 ›› Issue (2): 136-141.doi: 10.3760/cma.j.cn115500-20251229-26209

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Piezo1在青光眼眼压稳态及视神经损伤中的作用及机制

张琳昳1 魏金红2 刘建荣1 陈志宇1 熊思维1 王伟伟1   

  1. 1 西安市人民医院(西安市第四医院) 陕西省眼科医院,西安 710004;2 西北大学医学院,西安 710069
  • 收稿日期:2025-12-29 出版日期:2026-04-22 发布日期:2026-04-22
  • 通讯作者: 王伟伟,Email: hybweiwei@126.com
  • 基金资助:
    陕西省科技厅项目 (2022SF-434)

The role and mechanism of the piezo1 channel in intraocular pressure homeostasis and optic nerve injury in glaucoma

Zhang Linyi1, Wei Jinhong2, Liu Jianrong1, Chen Zhiyu1, Xiong Siwei1, Wang Weiwei1   

  1. 1 Shaanxi Eye Hospital, Xi’an People’s Hospital (Xi’an Fourth Hospital), Xi’an 710004, China;2 Northwest University Medical College, Xi’an 710069, China
  • Received:2025-12-29 Online:2026-04-22 Published:2026-04-22
  • Contact: Wang Weiwei, Email: hybweiwei@126.com
  • Supported by:
    Shaanxi Science and Technology Project (2022SF-434)

摘要: 青光眼是一类以视网膜神经节细胞(retinal ganglion cell, RGC)进行性丢失和视野缺损为特征的神经退行性疾病,眼压稳态失衡是重要危险因素,RGC损伤及视神经损害是核心病理特征。Piezo1作为机械敏感离子通道,在眼球关键组织中广泛表达,参与机械应力感知与信号转导。本文系统综述 Piezo1 通道在青光眼病理机制中参与眼压调控和RGC凋亡的双重作用:Piezo1通过调控钙离子信号通路、细胞外基质重塑及房水流出阻力,维持眼压稳态;Piezo1介导机械应力或缺血应激的钙依赖凋亡信号通路,参与RGC损伤。拟为青光眼的发病机制及新型干预策略提供理论依据。


关键词: Piezo1, 青光眼, 眼压稳态, 小梁网, 视神经损伤

Abstract: Glaucoma is a group of neurodegenerative disorders characterized by the progressive loss of retinal ganglion cells (RGCs) and visual field defects. Imbalance in intraocular pressure (IOP) homeostasis is an important risk factor, while RGC damage and optic nerve impairment are the core pathological features. As a mechanosensitive ion channel, Piezo1 is widely expressed in critical ocular tissues and mediates mechanosensory perception and signal transduction. This review systematically summarizes the dual role of the Piezo1 channel in glaucoma pathogenesis, specifically in IOP regulation and RGC apoptosis. We highlight that Piezo1 maintains IOP homeostasis by modulating calcium signaling pathways, extracellular matrix remodeling, and aqueous humor outflow resistance. Conversely, Piezo1 mediates calcium-dependent apoptotic signaling in response to mechanical stress or ischemic insults, thereby contributing to RGC injury. These insights provide a theoretical basis for investigating glaucoma pathogenesis and developing novel interventional strategies. 


Key words: Piezo1, Glaucoma, Intraocular pressure homeostasis, Trabecular meshwork, Optic nerve injury