How inflammation affects retinal repair in inherited vision loss
Inflammatory Signaling and Regeneration in Zebrafish models of Retinal Degeneration
This research explores if calming inflammation and changing two cellular signals (Notch and NF-kB) helps retinal support cells regrow light-sensing cells in inherited forms of vision loss.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | Cleveland Clinic Lerner Com-Cwru NIH-funded |
| Lab location | 1 site (Cleveland, United States) |
| Project ID | NIH-11263680 on NIH RePORTER |
What this research studies
From my perspective as a patient, the team uses zebrafish that model inherited retinal degenerations to learn why the fish cannot regenerate photoreceptors when inflammation is chronic. They compare responses after sudden injury versus ongoing degeneration, manipulate immune signals and Notch/NF-kB signaling, and watch whether Müller glia reprogram into progenitor cells that rebuild photoreceptors. The researchers use genetic zebrafish models (including cep290 and bbs2), immunosuppression experiments, and molecular assays such as ATAC-seq to track changes in gene regulation. Results aim to identify the inflammatory signals that block regeneration and point to targets that could be tested in future human therapies.
Who could benefit from this research
Good fit: Ideally this would ultimately apply to people with inherited retinal degenerations (for example certain forms of retinitis pigmentosa) who still retain some photoreceptors and may qualify for regenerative treatments in the future.
Not a fit: Patients with complete, long-standing loss of photoreceptors or vision from non-inherited causes are unlikely to benefit directly from this preclinical zebrafish research in the near term.
Why it matters
Potential benefit: If successful, this work could reveal targets to promote retinal repair or protect photoreceptors in people with inherited retinal degenerations.
How similar studies have performed: Similar approaches in zebrafish have shown that blocking Notch or modulating inflammation can enable regeneration, but linking microglia-driven inflammatory signals and NF-kB/Notch crosstalk as a reason regeneration fails in chronic degeneration is a newer idea.
Where this research is happening
Cleveland, United States
- Cleveland Clinic Lerner Com-Cwru — Cleveland, United States (Active)
Researchers
- Principal investigator: Perkins, Brian D — Cleveland Clinic Lerner Com-Cwru
- Study coordinator: Perkins, Brian D
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 below.