Understanding how lung cell toxicity contributes to a specific lung disease.
Official title: Elucidating the contribution of lung epithelial gain of function toxicity to AATD disease pathogenesis
Funded at Boston University Medical Campus · NIH-11046614 · Data updated 2026-11-12
This study is looking at how certain genetic factors affect lung health in people with alpha-1 antitrypsin deficiency (AATD), which can cause serious lung problems, to help find better ways to treat the condition.
Quick facts
| Grant type | P01 program project |
|---|---|
| Study type | NIH-funded research |
| Funding institution | Boston University Medical Campus NIH-funded |
| Lab location | 1 site (Boston, United States) |
| Project start | March 1, 2024 |
| Project end | February 28, 2029 |
| Funding year | 2025 |
| Award (this year) | $427,602 |
| NIH project number | 5P01HL170952-02 |
| Project ID | NIH-11046614 on NIH RePORTER |
Who could benefit from this research
✓Could help
Ideal candidates for this research are individuals diagnosed with alpha-1 antitrypsin deficiency, particularly those with the 'ZZ' genotype.
✕Less likely to help
Patients without alpha-1 antitrypsin deficiency or those with other unrelated lung conditions may not benefit from this research.
What this research studies
This research investigates the role of lung epithelial cell toxicity in the pathogenesis of alpha-1 antitrypsin deficiency (AATD), a genetic condition that can lead to severe lung disease. The study aims to explore how variations in genetic factors, particularly the 'ZZ' genotype, affect lung function and disease progression. By examining the balance between proteases and antiproteases in the lungs, the research seeks to identify additional contributors to lung injury beyond just low AAT levels. Patients with AATD may benefit from insights gained into the mechanisms of their disease, potentially leading to improved treatment strategies.
Why it matters
Potential benefit: If successful, this research could lead to better understanding and management of lung disease in patients with AAT deficiency.
How similar studies have gone: Previous research has shown varying success in understanding the mechanisms of AATD, but this specific approach to lung epithelial toxicity is relatively novel.
Where this research is happening
-
Boston University Medical Campus
Boston, United States Active
Researchers
- Principal investigator: Wilson, Andrew a — Boston University Medical Campus
- Study coordinator: Wilson, Andrew a
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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.