Abstract: Glaucoma is an ophthalmic disease characterized by optic nerve damage and visual field defects. Recent studies have revealed that ferroptosis, an iron-dependent form of regulated cell death driven by lipid peroxidation, is extensively involved in the pathogenesis of glaucoma. This article provides a systematic review of the molecular mechanisms and research progress on ferroptosis in the development and progression of glaucoma. Ferroptosis induces retinal ganglion cell death and trabecular meshwork dysfunction through iron metabolism dysregulation, accumulation of lipid peroxides, and aberrant regulation of key molecules such as GPX4. Significant alterations in ferroptosis-related markers have been observed in both animal models of glaucoma and clinical samples. Intervention strategies targeting key nodes of ferroptosis (e.g., GPX4, ACSL4, NCOA4), including iron chelators, small-molecule inhibitors, and gene therapy, have demonstrated clear neuroprotective and intraocular pressure-lowering effects in preclinical models. Ferroptosis intertwines with other pathological processes such as oxidative stress, excitotoxicity, and neuroinflammation, collectively driving glaucoma progression. Targeting ferroptosis offers a novel strategy for glaucoma treatment that extends beyond simple intraocular pressure reduction and holds significant potential for clinical translation.However, current evidence is mainly derived from animal models and in vitro experiments, and whether ferroptosis is a driver or a consequence of glaucoma remains to be clarified. A systems biology perspective integrating multiple signaling pathways may facilitate a more comprehensive understanding of the disease mechanisms.

Key words: Glaucoma, Neuroprotection, Ferroptosis