Functional genomic insights into epithelial dysfunction in pulmonary fibrosis
Official title: Project 3: Functional Genomic Mechanisms of Epithelial Dysfunction in Pulmonary Fibrosis
Funded at University of Michigan at Ann Arbor · NIH-11392456 · Data updated 2026-11-12
Researchers are studying people at risk for familial pulmonary fibrosis to understand how early cellular changes in the lungs develop into full disease.
Quick facts
| Grant type | P01 program project |
|---|---|
| Study type | NIH-funded research |
| Funding institution | University of Michigan at Ann Arbor NIH-funded |
| Lab location | 1 site (Ann Arbor, United States) |
| Project start | September 17, 2024 |
| Project end | July 31, 2029 |
| Funding year | 2026 |
| Award (this year) | $396,238 |
| NIH project number | 5P01HL172729-03 |
| Project ID | NIH-11392456 on NIH RePORTER |
Who could benefit from this research
✓Could help
Ideal candidates are individuals at risk for familial pulmonary fibrosis who undergo transbronchial biopsy as part of their clinical evaluation.
✕Less likely to help
Patients without access to advanced genomic testing or those not contributing biopsy samples may not directly benefit.
What this research studies
This project uses advanced gene-activity and chromatin-accessibility profiling on lung biopsy samples from people at risk for familial pulmonary fibrosis to map when and how epithelial cells change during early disease. By combining single-cell RNA sequencing with chromatin data, the team aims to link genetic variation to regulatory programs that shape the lung’s epithelial landscape. The study builds on pilot findings suggesting that detectable molecular shifts precede visible lung damage and may identify early targets for intervention.
Why it matters
Potential benefit: If successful, findings could enable earlier detection and pave the way for targeted therapies to slow or prevent disease progression in people at risk for familial PF.
How similar studies have gone: Preliminary single-nucleus multiomic data have shown disease-related regulatory changes, suggesting the approach is promising but still early.
Where this research is happening
-
University of Michigan at Ann Arbor
Ann Arbor, United States Active
Researchers
- Principal investigator: Kropski, Jonathan Andrew — University of Michigan at Ann Arbor
- Study coordinator: Kropski, Jonathan Andrew
Related research
Other NIH-funded projects on the same topics.
-
Molecular clues to progressive lung scarring
Researchers are studying how lung tissue becomes progressively scarred, focusing on cell signals and receptors that may drive fibrosis in people with lung disease.
-
Alveolar Cell Dysfunction in Pulmonary Fibrosis: Using SFTPC Mutations to Find New Targets
This grant explores how rare SFTPC mutations in alveolar cells may drive IPF and seeks new molecular targets to improve treatment.
-
Iron and scar-forming cells in the lungs (IPF)
Researchers are exploring how iron in the lungs may drive the scarring seen in idiopathic pulmonary fibrosis and whether this could lead to new therapies.
-
Repurposing Pyrvinium as an Inhaled Therapy for Idiopathic Pulmonary Fibrosis
A patient-friendly look at a project trying to use an existing drug, pyrvinium, as an inhaled treatment option for idiopathic pulmonary fibrosis (IPF).
-
Screening new compounds to reverse gene signatures in IPF lungs
A researcher hopes to find compounds that reverse harmful gene changes in the lungs of people with idiopathic pulmonary fibrosis (IPF).
-
Role of lactate transporters in lung scarring
Aims to see if blocking lactate transporters can slow or stop scar-forming cells from thickening the lungs in people with fibrotic lung disease.
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.