Protecting Eye Blood Vessels to Slow Vision Loss in Macular Degeneration

The goal of this project is to determine how loss of protective ETS factors damages choroidal blood vessels in AMD and to identify new strategies to preserve the choriocapillaris and prevent vision loss.

The choroid is a layer of blood vessels beneath the eye’s light-sensing neurons. It delivers the oxygen and nutrients needed for clear vision. In macular degeneration, these vessels slowly “wear out” under disease stress, much like tires that lose their tread over time. This process, called choroidal atrophy, deprives light-sensing cells of critical support and leads to vision loss. This project aims to uncover molecular pathways that protect these vessels from disease damage, supporting the BrightFocus mission to defeat macular degeneration.

This proposal is innovative because it focuses on protecting the choroidal blood vessels before irreversible retinal damage occurs in AMD. It identifies ETS transcription factors as newly recognized protectors of the choriocapillaris and tests TRIM25-mediated protein degradation as a potential cause of their loss. By combining genetic models, human donor tissues, and spatial transcriptomics, this project may uncover a new therapeutic strategy to slow or prevent AMD progression.

This proposal is innovative because it shifts the focus of AMD therapy from treating late-stage damage to preserving the choroidal blood vessels that support the outer retina. It identifies ETS transcription factors as previously underexplored protectors of the choriocapillaris and tests TRIM25-mediated protein degradation as a new mechanism driving choroidal atrophy. By combining genetic models and spatial transcriptomics, this project may reveal a new therapeutic pathway to slow or prevent AMD progression.