A newly identified artery muscle cell that may drive plaque buildup in atherosclerosis
Genomic Regulation and Translational Potential of a Novel Smooth Muscle Cell-Derived Cell Type in Atherosclerosis
This work looks at whether turning on vitamin A–related signals can stop artery muscle cells from changing into harmful cells that make plaque worse, aiming to help people with or at risk for atherosclerotic heart and blood vessel disease.
Quick facts
| Grant type | NIH-funded research |
|---|---|
| Study type | NIH-funded research |
| Funding institution | Vanderbilt University Medical Center NIH-funded |
| Lab location | 1 site (Nashville, United States) |
| Project ID | NIH-11254889 on NIH RePORTER |
What this research studies
Researchers are following a newly discovered smooth muscle–derived cell type that appears to promote inflammation and instability inside artery plaques. Using mouse models and single-cell gene profiling, they track how these cells form and what genes control their harmful behavior. The team is testing whether activating retinoic acid (a vitamin A–related pathway) can block the harmful cell transition and make plaques smaller and more stable. The findings could guide development of new treatments to reduce heart attack and stroke risk.
Who could benefit from this research
Good fit: People with atherosclerotic cardiovascular disease or at high risk for plaque buildup (for example, coronary, carotid, or peripheral artery disease) would be the most likely candidates to benefit from future therapies based on this work.
Not a fit: Patients whose conditions are not driven by atherosclerotic plaque (such as primary arrhythmias or congenital heart defects) or those needing immediate surgical care are unlikely to receive direct benefit from this preclinical research.
Why it matters
Potential benefit: If successful, this work could point to new therapies that slow plaque growth and make plaques less likely to cause heart attacks or strokes.
How similar studies have performed: Related animal studies, including the PI's prior mouse work, have shown that activating retinoic acid signaling can reduce plaque burden and improve cap stability, but this approach has not yet been proven in people.
Where this research is happening
Nashville, United States
- Vanderbilt University Medical Center — Nashville, United States (Active)
Researchers
- Principal investigator: Pan, Huize — Vanderbilt University Medical Center
- Study coordinator: Pan, Huize
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.