Understanding how fat signals and cell signals drive abnormal bone formation after injury or genetic conditions
Official title: Role of Leptin Receptor-STAT3 Signaling in Mesenchymal Progenitor Cell Fate Determination in Genetic and Traumatic Heterotopic Ossification
Funded at Texas A&m University Health Science Ctr · NIH-11447720 · Data updated 2026-11-12
A study to learn how a leptin-related signaling pathway affects the fate of mesenchymal cells that form bone in places they shouldn’t, with the goal of finding ways to prevent painful, abnormal bone growth.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | Texas A&m University Health Science Ctr NIH-funded |
| Lab location | 1 site (College Station, United States) |
| Project start | September 1, 2026 |
| Project end | August 31, 2031 |
| Funding year | 2026 |
| Award (this year) | $312,370 |
| NIH project number | 1R01AR086871-01A1 |
| Project ID | NIH-11447720 on NIH RePORTER |
Who could benefit from this research
✓Could help
Ideal candidates include individuals with or at risk for genetic or traumatic HO, such as patients with related genetic conditions or recent injuries that predispose to HO.
✕Less likely to help
Patients without HO or without risk factors for HO may not benefit from this research directly.
What this research studies
Researchers will examine how leptin receptor and STAT3 signaling influence mesenchymal progenitor cells as they decide whether to become bone cells in HO. The project uses genetic and injury-based mouse models, plus advanced genomic techniques like ATAC-seq to map chromatin accessibility and identify key regulatory steps. By linking specific signaling events to cell fate, the study aims to uncover therapeutic targets that could stop HO from forming or spreading after injury or in genetic diseases. This work could pave the way for new treatments that reduce pain and improve joint mobility for people affected by HO.
Why it matters
Potential benefit: If successful, the findings could lead to new therapies that prevent or limit heterotopic bone formation and improve quality of life for patients with HO.
How similar studies have gone: Previous studies in HO models support the involvement of signaling pathways and mesenchymal cells in abnormal bone formation, suggesting this approach is promising but still exploratory.
Where this research is happening
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Texas A&m University Health Science Ctr
College Station, United States Active
Researchers
- Principal investigator: Cong, Qian — Texas A&m University Health Science Ctr
- Study coordinator: Cong, Qian
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.