Targeting two retinal receptors linked to diabetic eye damage
Toward Targeting GPR31 and GPR39 Signaling in Diabetic Retinopathy
Testing whether blocking two retinal receptors (GPR31 and GPR39) can reduce inflammation and abnormal blood-vessel growth that harm vision in people with diabetic retinopathy.
Quick facts
| Grant type | R21 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | Oakland University NIH-funded |
| Lab location | 1 site (Rochester, United States) |
| Project ID | NIH-11182625 on NIH RePORTER |
What this research studies
If you have diabetes, this project looks at two specific receptors in the retina (GPR31 and GPR39) that respond to fat-derived molecules linked to inflammation. Researchers will use human retinal samples, lab-grown retinal cells (retinal endothelial cells and Müller cells), and diabetic mice to see whether these receptors drive inflammation, VEGF release, blood-retinal barrier breakdown, and abnormal vessel growth. They will map how the 12- and 15-HETE molecules bind to these receptors and trace the signaling steps that lead to vascular damage. Laboratory tests include molecular binding studies, cell signaling assays, and examination of retinal tissue for receptor expression and vascular changes.
Who could benefit from this research
Good fit: People with diabetic retinopathy—especially those showing signs of retinal blood-vessel leakage or abnormal new vessel growth—are the population most likely to benefit from therapies emerging from this research.
Not a fit: People without diabetic eye disease or those whose vision loss is from advanced scarring/fibrosis or non-diabetic causes are unlikely to benefit directly from this early-stage, lab-focused work.
Why it matters
Potential benefit: If successful, this work could point to new treatments that protect the retina and help prevent vision loss in diabetic retinopathy by targeting GPR31/GPR39.
How similar studies have performed: Prior animal studies blocking 12/15-lipoxygenase reduced blood-retinal barrier breakdown and neovascularization in mice, but directly targeting GPR31/GPR39 is a newer, less-tested approach.
Where this research is happening
Rochester, United States
- Oakland University — Rochester, United States (Active)
Researchers
- Principal investigator: Al-Shabrawey, Mohamed Al-Sayed — Oakland University
- Study coordinator: Al-Shabrawey, Mohamed Al-Sayed
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.