How clonal blood cell mutations drive artery disease
Mechanisms of Atherogenesis in Clonal Hematopoiesis
This project looks at whether a common blood mutation (JAK2V617F) and related inflammation make people with clonal hematopoiesis more likely to develop dangerous artery plaque.
Quick facts
| Grant type | NIH-funded research |
|---|---|
| Study type | NIH-funded research |
| Funding institution | University of California, San Francisco NIH-funded |
| Lab location | 1 site (San Francisco, United States) |
| Project ID | NIH-11166587 on NIH RePORTER |
What this research studies
Researchers use mouse models that carry the JAK2V617F mutation seen in people with clonal hematopoiesis to see how mutant blood cells affect artery plaques. They give antibodies that block the inflammatory molecule IL-1β to test whether this stops mutant macrophage proliferation and improves plaque stability. They apply single-cell RNA sequencing to identify inflammatory immune cells in lesions and study the role of the pyroptosis protein Gasdermin D in releasing IL-1β. The team aims to pinpoint inflammatory pathways driven by mutant blood cells that could be targeted to lower heart attack and stroke risk.
Who could benefit from this research
Good fit: People who have clonal hematopoiesis—particularly those with the JAK2V617F mutation—or those with early coronary artery disease risk would be the most relevant candidates for related future trials or sample donations.
Not a fit: People without clonal hematopoiesis or whose cardiovascular risk is driven only by traditional factors like uncontrolled cholesterol or smoking are less likely to benefit from these specific targeted approaches.
Why it matters
Potential benefit: If successful, the work could point to treatments (for example IL-1β–targeting therapies or interventions affecting Gasdermin D pathways) that reduce heart attack and stroke risk in people with clonal hematopoiesis.
How similar studies have performed: Previous human trials targeting IL-1β (for example CANTOS) have reduced heart attacks, supporting the idea that blocking IL-1β can help, while applying this specifically to JAK2-driven clonal hematopoiesis is a newer, less-tested direction.
Where this research is happening
San Francisco, United States
- University of California, San Francisco — San Francisco, United States (Active)
Researchers
- Principal investigator: Fidler, Trevor Perawaskin Laramee — University of California, San Francisco
- Study coordinator: Fidler, Trevor Perawaskin Laramee
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.