Research progress of ferroptosis in glaucoma and optic nerve damage

Unlike other death forms, such as autophagy, necrosis, and apoptosis, ferroptosis is a novel type of programmed cell death with iron-dependent properties. Esteroxygenase affects the content of unsaturated fatty acids and promotes lipid peroxidation. In addition, GSH can cause the reduction of GPX4, which can cause ferroptosis. P53 and its signaling pathways also regulate ferroptosis. Recent studies have confirmed that ferroptosis also promotes the death of RGC. The progressive loss of RGC is one of the pathological features of glaucoma, indicating that ferroptosis may be related to the onset of glaucoma. Down-regulation of GPX4 leads to the loss of nerve cells, which suggests that ferroptosis may also be related to diseases related to optic nerve damage. At present, ferroptosis has been extensively researched and advanced in systemic diseases, such as cardiovascular diseases, gastrointestinal tumors such as stomach, liver, and pancreas, and brain diseases. This review focuses on the research progress of ferroptosis in ophthalmic diseases, especially glaucoma and optic nerve damage.