Controlling inflammation and scarring to repair large muscle loss
Official title: Engineering the Immune and Fibrotic Response in Volumetric Muscle Loss
Funded at University of Oregon · NIH-11395064 · Data updated 2026-11-12
Develops ways to control inflammation and scarring to help people with large traumatic muscle loss heal stronger and with less pain.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | University of Oregon NIH-funded |
| Lab location | 1 site (Eugene, United States) |
| Project start | September 16, 2021 |
| Project end | August 31, 2026 |
| Funding year | 2025 |
| Award (this year) | $89,294 |
| NIH project number | 3R01AR078375-05S1 |
| Project ID | NIH-11395064 on NIH RePORTER |
Who could benefit from this research
✓Could help
People with significant traumatic volumetric muscle loss—such as from battlefield injuries, severe limb trauma, or surgical removal of large muscle segments—would be the ideal candidates.
✕Less likely to help
People with minor muscle strains, chronic non-traumatic muscle diseases without large tissue loss, or medical conditions that prevent regenerative therapies are unlikely to benefit from this work.
What this research studies
This project looks at why large, full-thickness muscle injuries fail to regrow and instead form scar and fat that limit function. Researchers study how support cells called fibro-adipogenic progenitors (FAPs) and immune signals drive that harmful response using laboratory and animal models. They will test engineered approaches to change the local immune and fibrotic environment so muscle stem cells can rebuild tissue rather than producing scar or fat. The work is intended to identify strategies that could later be translated into therapies for people with volumetric muscle loss.
Why it matters
Potential benefit: Could lead to treatments that reduce scarring and fatty replacement and restore muscle strength and function after severe traumatic muscle loss.
How similar studies have gone: Related preclinical work altering immune signals and FAP behavior has shown promise in reducing fibrosis and improving repair, but translating those findings into human treatments is still experimental.
Where this research is happening
-
University of Oregon
Eugene, United States Active
Researchers
- Principal investigator: Willett, Nick J — University of Oregon
- Study coordinator: Willett, Nick J
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.