This is a long review of this big problem. It looks like Prof Finkelstein together with Dr. C Nguyen are doing something in this area. They have published a paper: "Effects of Excess Iron on the Retina: Insights From Clinical Cases and Animal Models of Iron Disorders". I am hopeful that something will come out of this cooperation.

It looks like an iron chelation drug will one day be needed. ATH434 eye drops, I hope.

This is a free paper, here is the abstract.

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Review

Front Endocrinol (Lausanne)

. 2023 Sep 13;14:1234824.

doi: 10.3389/fendo.2023.1234824. eCollection 2023.

Spotlight on iron and ferroptosis: research progress in diabetic retinopathy

Junlin Ouyang ¹, Ling Zhou ², Qing Wang ¹

Affiliations expand

• PMID: 37772084

PMCID: PMC10525335 DOI: 10.3389/fendo.2023.1234824Free PMC article

Abstract

Iron, as the most abundant metallic element within the human organism, is an indispensable ion for sustaining life and assumes a pivotal role in governing glucose and lipid metabolism, along with orchestrating inflammatory responses. The presence of diabetes mellitus (DM) can induce aberrant iron accumulation within the corporeal system. Consequentially, iron overload precipitates a sequence of important adversities, subsequently setting in motion a domino effect wherein ferroptosis emerges as the utmost pernicious outcome. Ferroptosis, an emerging variant of non-apoptotic regulated cell death, operates independently of caspases and GSDMD. It distinguishes itself from alternative forms of controlled cell death through distinctive morphological and biochemical attributes. Its principal hallmark resides in the pathological accrual of intracellular iron and the concomitant generation of iron-driven lipid peroxides. Diabetic retinopathy (DR), established as the predominant cause of adult blindness, wields profound influence over the well-being and psychosocial strain experienced by afflicted individuals. Presently, an abundance of research endeavors has ascertained the pervasive engagement of iron and ferroptosis in the microangiopathy inherent to DR. Evidently, judicious management of iron overload and ferroptosis in the early stages of DR bears the potential to considerably decelerate disease progression. Within this discourse, we undertake a comprehensive exploration of the regulatory mechanisms governing iron homeostasis and ferroptosis. Furthermore, we expound upon the subsequent detriments induced by their dysregulation. Concurrently, we elucidate the intricate interplay linking iron overload, ferroptosis, and DR. Delving deeper, we engage in a comprehensive deliberation regarding strategies to modulate their influence, thereby effecting prospective interventions in the trajectory of DR's advancement or employing them as therapeutic modalities.