Abstract

AbstractIron has a dual role. Essential for cellular functions, it enhances oxidative stress when it is in excess and under a labile form. Iron accumulation and iron balance dysregulation are observed in animal models of retinal degeneration. Recently, we observed iron overload in ocular fluids from retinal detachment patients and highly transferrin saturation. As therapeutic strategy, we used transferrin (TF), the physiological iron transporter and the second most abundant protein in the vitreous, to reduce iron overload and therefore preserve visual function. Ocular administration of TF was no toxic. By several delivery ways and in different animal models of retinal dystrophies, we demonstrated the beneficial effect of TF. Iron accumulation, inflammation, oxidative stress, edema and cell death were decreased and retinal histology and visual function were preserved. Control of iron impairment in retinal tissues may be a major therapeutic strategy. We highlight the therapeutic potential of Transferrin in retinal diseases preventing vision loss.

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