Endothelial C3a Receptor's Role in Stroke-Related Brain Injury
Official title: Endothelial complement C3a receptor mediated cerebral injury in a murine stroke model.
Funded at St. Joseph's Hospital and Medical Center · NIH-11170634 · Data updated 2026-11-12
Aims to understand how a specific immune signal (C3a receptor on blood vessel lining) worsens brain damage after stroke, with the goal of improving outcomes after clot-busting therapy.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | St. Joseph's Hospital and Medical Center NIH-funded |
| Lab location | 1 site (Phoenix, United States) |
| Project start | September 1, 2024 |
| Project end | August 31, 2030 |
| Funding year | 2026 |
| Award (this year) | $701,372 |
| NIH project number | 5R01NS138528-02 |
| Project ID | NIH-11170634 on NIH RePORTER |
Who could benefit from this research
✓Could help
Ideal candidates are adults with or at risk for ischemic stroke or those who could benefit from therapies that protect the brain after clot-busting treatment.
✕Less likely to help
This study uses mouse models; direct benefits to current patients would require future human trials and translation.
What this research studies
This project studies how the C3a receptor on brain blood vessels contributes to brain injury after a stroke and how blocking it might protect the brain. Researchers will use mouse models to test whether inhibiting endothelial C3aR reduces blood-brain barrier breakdown, inflammation, and loss of brain connections after stroke. The study will measure neurological function, barrier integrity, and tissue changes over several weeks to months, aiming to translate findings toward safer, more effective treatments for stroke patients receiving clot-busting therapy. If successful, this work could pave the way for a new therapeutic approach to limit secondary brain injury after stroke.
Why it matters
Potential benefit: If successful, this research could lead to therapies that protect the brain after stroke and improve recovery.
How similar studies have gone: Previous work supports the idea that immune signals contribute to brain injury after stroke, with potential for targeted therapies to reduce damage.
Where this research is happening
-
St. Joseph's Hospital and Medical Center
Phoenix, United States Active
Researchers
- Principal investigator: Ducruet, Andrew Frederick — St. Joseph's Hospital and Medical Center
- Study coordinator: Ducruet, Andrew Frederick
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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.