Abstract: Ferroptosis is a form of iron-dependent, lipid peroxidation-driven cell death. Under conditions of iron overload, glutathione peroxidase becomes inactivated, leading to the accumulation of intracellular lipid peroxides. This triggers severe damage to mitochondria and cell membranes, ultimately resulting in cell death. Diabetic retinopathy (DR) arises from interactions among apoptosis, endothelial hyperplasia, and neuronal apoptosis. Ferroptosis can influence DR pathogenesis through multiple pathways, including iron metabolism dysregulation, abnormal amino acid metabolism, and mitochondrial damage caused by the accumulation of lipid peroxide radicals. Targeted regulation of ferroptosis pathways offers a novel direction for the treatment of DR.

Key words: Ferroptosis, Diabetic retinopathy, Iron metabolism