Targeting a specific receptor to improve treatment for lung fibrosis
Official title: Targeting Fibroblast Discoidin Domain Receptor 2 for Immunotherapy to Pulmonary Fibrosis
Funded at University of Michigan at Ann Arbor · NIH-10983754 · Data updated 2026-11-12
This study is looking at a protein called DDR2 that might play a big role in worsening lung scarring in people with progressive pulmonary fibrosis, and by focusing on this protein, researchers hope to create better treatments that could help you breathe easier and feel better.
Quick facts
| Grant type | R01 grant |
|---|---|
| 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 | December 1, 2021 |
| Project end | November 30, 2025 |
| Funding year | 2025 |
| Award (this year) | $544,792 |
| NIH project number | 5R01HL156998-04 |
| Project ID | NIH-10983754 on NIH RePORTER |
Who could benefit from this research
✓Could help
Ideal candidates for this research are individuals diagnosed with progressive pulmonary fibrosis or related lung conditions.
✕Less likely to help
Patients with non-fibrotic lung diseases or those who do not have a diagnosis of pulmonary fibrosis may not benefit from this research.
What this research studies
This research focuses on improving therapies for progressive pulmonary fibrosis, a serious lung condition. It investigates the role of discoidin domain receptor 2 (DDR2), a specific protein found in fibroblasts, which may be crucial in driving fibrosis. By targeting DDR2, the research aims to develop more effective treatments that can specifically inhibit the pathways leading to lung scarring. Patients may benefit from a more tailored approach to therapy that could lead to better outcomes than current treatments.
Why it matters
Potential benefit: If successful, this research could lead to more effective treatments for patients suffering from pulmonary fibrosis.
How similar studies have gone: Previous research has shown promise in targeting specific receptors for treating fibrosis, indicating potential success for this approach.
Where this research is happening
-
University of Michigan at Ann Arbor
Ann Arbor, United States Active
Researchers
- Principal investigator: Kim, Kevin Keewoun — University of Michigan at Ann Arbor
- Study coordinator: Kim, Kevin Keewoun
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.