Understanding how tobacco smoke changes lung fibroblasts in pulmonary fibrosis
Official title: Deciphering Tobacco Smoke-Driven Fibroblast Reprogramming in Pulmonary Fibrosis
Funded at University of California at Davis · NIH-11443942 · Data updated 2026-11-12
A study exploring how cigarette smoke affects lung cells to drive fibrosis, with a focus on a protein called PRMT5 and potential ways to slow disease progression.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | University of California at Davis NIH-funded |
| Lab location | 1 site (Davis, United States) |
| Project start | September 1, 2026 |
| Project end | May 31, 2030 |
| Funding year | 2026 |
| Award (this year) | $770,045 |
| NIH project number | 1R01HL187988-01 |
| Project ID | NIH-11443942 on NIH RePORTER |
Who could benefit from this research
✓Could help
Ideal candidates are adults with or at risk for idiopathic pulmonary fibrosis or smoking-related fibrotic lung disease, especially those whose cells can be studied in the lab.
✕Less likely to help
Patients without fibrotic lung disease or those not contributing biological samples may not directly benefit.
What this research studies
This work looks at the ways tobacco smoke may cause lung scarring by changing fibroblasts in the lungs. Researchers will use proteomic and metabolomic profiling to identify key molecular changes, especially involving lactylation and PRMT5, and test how inhibiting PRMT5 affects cell growth and invasiveness. Results could point to new targets for therapies that slow or prevent fibrotic remodeling in patients with smoking-related lung disease. The study is conducted with human-derived lung cells and tissues to ground findings in human biology.
Why it matters
Potential benefit: If successful, the work could lead to new treatments that reduce lung scarring and improve outcomes for patients with smoke-related pulmonary fibrosis.
How similar studies have gone: Preliminary data in human lung cells suggest PRMT5 involvement in fibrotic behaviors and inhibition reduces these traits in vitro, indicating potential, though clinical benefit is not yet proven.
Where this research is happening
-
University of California at Davis
Davis, United States Active
Researchers
- Principal investigator: Chen, Ching-Hsien — University of California at Davis
- Study coordinator: Chen, Ching-Hsien
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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.