Blood-cell mutations and inflammation that speed artery plaque buildup
Clonal hematopoiesis, inflammasomes and atherosclerosis
['FUNDING_R01'] · COLUMBIA UNIVERSITY HEALTH SCIENCES · NIH-11252528
This project looks at whether mutated blood cells drive inflammation that worsens artery plaque and heart disease in people with clonal hematopoiesis.
Quick facts
| Phase | ['FUNDING_R01'] |
|---|---|
| Study type | Nih_funding |
| Sex | All |
| Sponsor | COLUMBIA UNIVERSITY HEALTH SCIENCES (nih funded) |
| Locations | 1 site (NEW YORK, UNITED STATES) |
| Trial ID | NIH-11252528 on ClinicalTrials.gov |
What this research studies
Researchers will use mouse models that carry the common clonal hematopoiesis mutations (like TET2 loss and JAK2V617F) and experiments with human blood cells to see how inflammasomes such as AIM2 and NLRP3 trigger inflammatory signals in artery plaques. They will track whether mutant cells cause nearby normal immune cells to become inflamed through IL-1β and related pathways, and measure plaque growth and immune changes in mice. The team will also test whether blocking these inflammasome or IL-1β signals reduces inflammation and plaque, and will compare results with human cell samples to identify possible treatment targets.
Who could benefit from this research
Good fit: People with clonal hematopoiesis—especially those known to carry TET2 or JAK2 mutations or who have an elevated risk of atherosclerotic cardiovascular disease—would be the most relevant candidates to contribute samples or be considered for related future trials.
Not a fit: People without clonal hematopoiesis or whose cardiovascular disease is driven by unrelated causes may not see direct benefit from findings focused on these specific blood-cell mutations.
Why it matters
Potential benefit: If successful, this work could point to new anti-inflammatory treatments (for example targeting inflammasomes or IL-1β) to lower heart and vascular risk in people with clonal hematopoiesis.
How similar studies have performed: Prior work has shown that blocking IL-1β reduces heart attack risk and that TET2/JAK2 mutations link to inflammation, but applying targeted AIM2/NLRP3-based therapies specifically for clonal hematopoiesis is still a new and developing approach.
Where this research is happening
NEW YORK, UNITED STATES
- COLUMBIA UNIVERSITY HEALTH SCIENCES — NEW YORK, UNITED STATES (ACTIVE)
Researchers
- Principal investigator: TALL, ALAN RICHARD — COLUMBIA UNIVERSITY HEALTH SCIENCES
- Study coordinator: TALL, ALAN RICHARD
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 below.