This paper below explains the pathology of subretinal hemorrhage, most commonly manifested as a complication of exudative age-related macular degeneration and often leads to blindness. The paper is free to read. It also explains how an iron chelator (Deferoxamine) could work the problem but tells also the known side-effects of that drug. So a safer option, as I think ATH434, could work ???? But this is a very big and complex problem and needs a lot of research. Maybe Prof Finkelstein is planning something with ATH434????

Review

Biomed Pharmacother

. 2023 Sep 22;167:115572.

doi: 10.1016/j.biopha.2023.115572. Online ahead of print.

A systematic review of the cell death mechanisms in retinal pigment epithelium cells and photoreceptors after subretinal hemorrhage - Implications for treatment options

Sirjan Chhatwal ¹, Henrike Antony ¹, Saman Lamei ¹, Tamás Kovács-Öller ², Alexa Karina Klettner ³, Marietta Zille ⁴

Affiliations expand

• PMID: 37742603

DOI: 10.1016/j.biopha.2023.115572Free article

Abstract

Humans rely on vision as their most important sense. This is accomplished by photoreceptors (PRs) in the retina that detect light but cannot function without the support and maintenance of the retinal pigment epithelium (RPE). In subretinal hemorrhage (SRH), blood accumulates between the neurosensory retina and the RPE or between the RPE and the choroid. Blood breakdown products subsequently damage PRs and the RPE and lead to poor vision and blindness. Hence, there is a high need for options to preserve the retina and visual functions. We conducted a systematic review of the literature in accordance with the PRISMA guidelines to identify the cell death mechanisms in RPE and PRs after SRH to deepen our understanding of the pathways involved. After screening 736 publications published until November 8, 2022, we identified 19 records that assessed cell death in PRs and/or RPE in experimental models of SRH. Among the different cell death mechanisms, apoptosis was the most widely investigated mechanism (11 records), followed by ferroptosis (4), whereas necroptosis, pyroptosis, and lysosome-dependent cell death were only assessed in one study each. We discuss different therapeutic options that were assessed in these studies, including the removal of the hematoma/iron chelation, cytoprotection, anti-inflammatory agents, and antioxidants. Further systematic investigations will be necessary to determine the exact cell death mechanisms after SRH with respect to different blood breakdown components, cell types, and time courses. This will form the basis for the development of novel treatment options for SRH.