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Figure 1. 

Dynamic microglial activation in traditional or novel classification. The static microglia serve as guardians that monitor the microenvironment and are activated into different subtypes in glaucoma. Historically, the M1/M2 paradigm established for macrophages has been applied to microglial classification. The M1 phenotype mediates pro-inflammatory responses via cytotoxic factors and inflammasomes, leading to RGC loss, while M2 phenotype plays a neuroprotective role in promoting RGC survival. Advances in high-throughput technologies enabled identification of more precise microglial subpopulations: CD74⁺ microglia from DAM drive neuroinflammation whereas LXB₄ treatment promote their transformation to homeostatic microglia; MGnD (Lgal3⁺ microglia) can be suppressed by APOE4 upregulation, thereby contributing to RGC protection. Notably, MGnD may be derived from DAM or coexistence with DAM.

Figure 2. 

Müller cells play a role in microglial proliferation and the migration of Müller cells are mainly involved in the proliferation and migration of microglia through ATP releasing and primarily mediate P2X7R and P2X4R on microglia. In addition, after being stimulated by microglia, Müller cells release sufficient adhesion factors to attract microglia, promoting their vertical migration across the retina to GCL.

Figure 3. 

A network of the interplay between microglia and intraretinal cell in glaucoma. Microglia interplay with a variety of retinal cells. RGCs, Müller cells, and astrocytes are the leading interactive cells when oligodendrocytes are also affected to a small extent. These interactions affect the microglial function, lead to neuroprotective or neurodegenerative lesions, and ultimately affect pathological outcomes within glaucoma. The interplay of other retina cells with microglia is mainly reflected in other disease models and awaits further explanations in glaucoma.