BackgroundDiabetic retinopathy (DR) is a significant complication of diabetes and the primary cause of blindness among working age adults globally. The development of DR is accompanied by oxidative stress, characterised by an overproduction of reactive oxygen species (ROS) and a compromised antioxidant system. Clinical interventions aimed at mitigating oxidative stress through ROS scavenging or elimination are currently available. Nevertheless, these treatments merely provide limited management over the advanced stage of the illness. Ferroptosis is a distinctive form of cell death induced by oxidative stress, which is characterised by irondependent phospholipid peroxidation.PurposeThis review aims to synthesise recent experimental evidence to examine the involvement of ferroptosis in the pathological processes of DR, as well as to explicate the regulatory pathways governing oxidative stress and ferroptosis in retina.MethodsWe systematically reviewed literature available up to 2023.ResultsThis review included 12 studies investigating the involvement of ferroptosis in DR. Schematic diagram of potential pathways leading to DR caused by ferroptosis. Characteristic manifestations of DR in the retina include haemorrhage, hard exudation, angiogenesis, and neurodegeneration. Iron accumulation, lipid peroxidation, and impaired antioxidant defence systems induced ferroptosis in diabetic retinopathy, resulting in compromised retinal cell viability, disrupted cell-to-cell junctions, and elicited inflammatory responses.