Faulty TRPV4–eNOS signaling in the eye's drainage tissue linked to glaucoma
Impaired TRVP4-eNOS signaling in TM contributes to glaucoma
Looking at whether restoring a damaged pressure-sensing pathway in the eye's drainage tissue can help people with primary open-angle glaucoma control eye pressure.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | University of California-Irvine NIH-funded |
| Lab location | 1 site (Irvine, United States) |
| Project ID | NIH-11136881 on NIH RePORTER |
What this research studies
From a patient's point of view, researchers will study the trabecular meshwork (the eye's drainage tissue) using cells and donor eye tissue to see why a pressure-sensing pathway (TRPV4–eNOS) stops working in glaucoma. They will measure how endoplasmic reticulum (ER) stress and an inflammatory enzyme (iNOS) raise harmful molecules like peroxynitrite that damage the TRPV4 channel. The team will test ways to block or reverse those damaging signals in lab models and human-derived cells to try to restore normal channel function. The goal is to identify targets or treatments that could someday protect or improve the drainage tissue's ability to control intraocular pressure.
Who could benefit from this research
Good fit: People with primary open-angle glaucoma, particularly those with elevated intraocular pressure or known trabecular meshwork dysfunction, or patients willing to donate eye tissue for research, would be most relevant to this work.
Not a fit: Patients seeking immediate clinical treatment or those with non–open-angle glaucoma types are unlikely to receive direct or immediate benefit from this lab-focused research.
Why it matters
Potential benefit: If successful, this work could identify new ways to protect or restore drainage-tissue function and reduce the high eye pressure that causes vision loss in primary open-angle glaucoma.
How similar studies have performed: Prior work (including the investigators' preliminary data) showed TRPV4–eNOS signaling can lower eye pressure and is impaired in glaucomatous tissue, but targeting ER stress/iNOS to rescue this pathway is a newer approach.
Where this research is happening
Irvine, United States
- University of California-Irvine — Irvine, United States (Active)
Researchers
- Principal investigator: Zode, Gulab — University of California-Irvine
- Study coordinator: Zode, Gulab
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.