REVIEW article
Front. Immunol.
Sec. Inflammation
This article is part of the Research TopicRetinal Degenerative Diseases: Processes and Potential TreatmentsView all 10 articles
The Role of Microglia in Glaucoma - Trigger and Potential Target
Provisionally accepted
- Renmin Hospital of Wuhan University, Wuhan, China
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Glaucoma is a neurodegenerative disease characterized by the progressive loss of retinal ganglion cell and optic nerve damage. Recent studies have highlighted the pivotal role of microglia in the onset and progression of glaucoma. This review aims to elucidate the key mechanisms of microglial activation in glaucoma and assess its potential as a therapeutic target for novel treatment strategies. Microglia activation in glaucoma is multifactorial, driven by biomechanical, metabolic, and inflammatory signals. Activated microglia contribute to both neuroinflammatory injury and neuroprotective responses. Their interaction with other kinds of cell establishes a dynamic inflammatory signaling network that exacerbates retinal ganglion cell loss. Furthermore, emerging evidence suggests that key targets in microglial activation, such as APOE, LGALS3, CX3CR1, etc play critical roles in disease progression, revealing promising targets for therapeutic intervention. Microglia act as central regulators of the retinal immune microenvironment in glaucoma. Their dual role in neurotoxicity and neuroprotection is shaped by complex interactions with other kinds of cell. Targeting microglial activation state and restoring metabolic homeostasis represent promising strategies for the development of pressure-independent treatments for glaucoma.
Keywords: Glaucoma, High intraocular pressure, Microglia, retinal ganglion cell, Intercellularcommunications
Received: 14 Aug 2025; Accepted: 27 Oct 2025.
Copyright: © 2025 Chen, Yang, Wang and Huang. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Pingping Huang, 283531363@qq.com
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