A Paris-based research report suggests that transferrin, the iron-binding serum protein, could be useful to help to treat patients with retinal detachment (RD). Human studies indicate that ocular fluids from patients with rhegmatogenous retinal detachment (RRD) shows that iron increases with detachment duration and correlates with poor visual recovery. While there is clear progress made in surgical techniques for RRD treatment, at present RRD patients have poor vision-related quality of life therefore there is a critical therapeutic challenge. A strategy for a treatment could involve a supplementation of transferrin activity to neutralize iron toxicity and may restore iron homeostasis in animal models.
Research in model disease studies show that iron (FeSO4) induces photoreceptor cell death in retinal explants and that transferrin protects activity against iron-induced toxicity. Following research, transferrin (using a transgenic model expressing human transferrin) can rescue the detached retina in vivo and thereafter, local ocular injection of transferrin preserves detached retinas in animal models. These results indicate that “therapeutic TF (transferrin) thus reduced edema of the detached retina and preserved PR (photoreceptor) morphology. Together, these results indicate that TF, even if administrated at the time of RD (retinal degeneration), can prevent further retinal alterations and cell death”.
On a considerable volume of studies of the results, the researchers state that, “we proposed to use local ocular TF to neutralize iron toxicity. We previously showed that TF is safe for ocular use even at high doses and prevents iron accumulation in RPE and PRs, and that iron-loaded (holoTF) and iron-free TF egresses the retina through the TF receptor at the RPE apical side”. In essence, the study shows that transferrin supplementation may provide a credible strategy for “further translational clinical trials in eligible patients” and that transferrin treatment “not only restores iron homeostasis but also activates major neuroprotective pathways”.