Glaucoma is a chronic neurodegenerative disorder characterized by progressive optic nerve damage and visual field loss. Its pathogenesis is complex and has not yet been fully elucidated. In recent years, accumulating evidence has suggested that microglia, as important resident immune cells in the retina, play a critical role in glaucoma-related neuroinflammation, retinal ganglion cell(RGC)injury, and disease progression. Notably, the role of microglia in glaucoma does not appear to be unidirectionally deleterious; rather, it may exhibit marked temporal heterogeneity and dual effects. Early microglial responses may help maintain tissue homeostasis and promote debris clearance, whereas persistent or excessive activation may aggravate RGC damage through the release of pro-inflammatory mediators, amplification of intercellular signaling, and remodeling of the local immune microenvironment. Meanwhile, with the development of optical coherence tomography(OCT)and optical coherence tomography angiography(OCTA), researchers have been able to visualize and quantify macrophage-like cells(MLCs)in vivo at the vitreoretinal interface(VRI). MLCs are considered to be associated with retinal immune activation; however, their precise cellular identity and the specific significance in glaucoma remain to be further clarified. This review summarizes the mechanisms of microglia in neuroinflammation underlying glaucoma and their relationship with RGC injury, and further discusses the potential origins of MLCs, the methodology of en face OCT/OCTA imaging, and recent advances in their potential application as imaging biomarkers, aiming to provide a reference for the early identification and monitoring of glaucoma, as well as for the pressure-independent intervention strategies.

国家自然科学基金资助项目(No.82471075)