How a blood protein (eNAMPT) and immune signaling harm blood vessels in severe lung failure (ARDS)
Official title: Role of Endothelial eNAMPT/NAMPT secretion and TLR4 signaling in the ARDS Vascular Endotype
Funded at University of Florida · NIH-11193838 · Data updated 2026-11-12
Looks at whether blocking a blood protein called eNAMPT can reduce blood-vessel inflammation and leakage in people with severe lung failure (ARDS).
Quick facts
| Grant type | P01 program project |
|---|---|
| Study type | NIH-funded research |
| Funding institution | University of Florida NIH-funded |
| Lab location | 1 site (Gainesville, United States) |
| Project start | September 20, 2016 |
| Project end | August 31, 2027 |
| Funding year | 2025 |
| Award (this year) | $299,983 |
| NIH project number | 5P01HL126609-09 |
| Project ID | NIH-11193838 on NIH RePORTER |
Who could benefit from this research
✓Could help
Adults with acute respiratory distress syndrome (ARDS), including ARDS related to infection or mechanical ventilation, would be the most relevant candidates.
✕Less likely to help
People without ARDS or with mild lung injury not driven by vascular inflammation are unlikely to benefit from this approach.
What this research studies
This project focuses on a protein called eNAMPT that is released into the blood during severe lung injury and may drive blood-vessel inflammation and leakage. Researchers measure eNAMPT levels in patient blood samples and use animal models (mice, rats, pigs) to test how eNAMPT and its signaling through TLR4 cause lung vascular injury. They test whether neutralizing eNAMPT or interrupting its signaling can prevent or reduce lung blood-vessel leak and inflammation in preclinical models. The team aims to link the biomarker findings to possible therapies that could protect blood vessels in ARDS.
Why it matters
Potential benefit: If successful, this work could lead to treatments that reduce lung blood-vessel leak and inflammation and lower ARDS severity and deaths.
How similar studies have gone: Preclinical studies in mice, rats, and pigs have shown promising protection from targeting eNAMPT, but human clinical trials are limited or not yet established.
Where this research is happening
-
University of Florida
Gainesville, United States Active
Researchers
- Principal investigator: Garcia, Joe G. N. — University of Florida
- Study coordinator: Garcia, Joe G. N.
Related research
Other NIH-funded projects on the same topics.
-
Coordinating ARDS, Pneumonia, and Sepsis research to improve care
A national coordinating center helps researchers studying ARDS and related infections work together more efficiently to learn what helps patients recover.
-
Lipid-gene Profiles in Septic ARDS
A Mayo Clinic team is studying how dysfunctional HDL in sepsis relates to different ARDS patient outcomes, aiming to find features that could guide better treatment.
-
Improving blood vessel repair after pediatric ARDS
Aims to better repair the lungs of children who have ARDS by delivering targeted therapy to lung blood vessels using tiny nanoparticles.
-
NOX4 links to ARDS risk and progression
Aims to understand how NOX4-driven cell damage may make some adults with ARDS worse off and how this could lead to earlier, targeted care.
-
Leading causes of death in alcoholic ARDS patients using clinical data
This project uses big clinical data and AI to find the main factors that cause death in adults with ARDS who have alcohol use issues, aiming to improve understanding and care.
-
Targeting aging-related blood vessel injury to prevent ARDS in older lungs
Aims to find ways to protect lung blood vessels in older adults to prevent dangerous lung swelling (ARDS).
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.