How oxidative stress may cause Fuchs endothelial corneal dystrophy
Official title: Role of Oxidative Stress in Pathogenesis of Fuchs Endothelial Corneal Dystrophy
Funded at Schepens Eye Research Institute · NIH-11141733 · Data updated 2026-11-12
This research looks at whether oxidative stress from aging, UV-A light, and smoking harms corneal endothelial cells and leads to Fuchs dystrophy, especially in older women.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | Schepens Eye Research Institute NIH-funded |
| Lab location | 1 site (Boston, United States) |
| Project start | July 1, 2010 |
| Project end | July 31, 2029 |
| Funding year | 2025 |
| Award (this year) | $602,106 |
| NIH project number | 5R01EY020581-16 |
| Project ID | NIH-11141733 on NIH RePORTER |
Who could benefit from this research
✓Could help
People diagnosed with Fuchs endothelial corneal dystrophy—particularly older adults, women, and those with a history of smoking or significant UV exposure—would be most relevant to this research.
✕Less likely to help
People without FECD or those whose disease is already end-stage and awaiting corneal transplant are unlikely to directly benefit from this mechanistic research in the short term.
What this research studies
Researchers are studying how aging, UV-A exposure, and smoking upset the balance between oxidants and antioxidants in corneal endothelial cells and lead to the cell loss and guttae seen in Fuchs dystrophy. They will use lab models (cells and mice) and molecular tests to examine mitochondrial DNA damage, cell cycle arrest, polyploidy, and abnormal extracellular matrix that cause corneal scarring. The team will probe hormone-related enzymes and receptors (such as AhR and CYP1B1) and changes in melatonin chemistry that may make female eyes more vulnerable. This work builds on earlier findings linking oxidative DNA damage and mitochondrial dysfunction to FECD.
Why it matters
Potential benefit: If successful, the findings could point to new ways to protect corneal endothelial cells or prevent the guttae and scarring that lead to vision loss.
How similar studies have gone: Previous studies, including the investigators' own work, have linked oxidative and mitochondrial DNA damage to FECD, but the proposed AhR/CYP1B1–melatonin pathway and its connection to guttae formation are relatively novel.
Where this research is happening
-
Schepens Eye Research Institute
Boston, United States Active
Researchers
- Principal investigator: Jurkunas, Ula V. — Schepens Eye Research Institute
- Study coordinator: Jurkunas, Ula V.
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About this research
- This is an active NIH-funded research project — typically early-stage science, not a clinical trial accepting patient enrollment.
- Some NIH-funded labs run parallel clinical studies or seek volunteers for related work. To check, contact the principal investigator or institution listed above.
- For full project details, budget, and progress reports, visit the official NIH RePORTER page.