How artery wall muscle cells change and affect heart disease risk
Gene regulatory networks controlling smooth muscle phenotype and vasculardisease risk
Researchers are looking at gene switches in artery muscle cells to understand how they drive atherosclerosis and coronary artery disease for people with or at risk of these conditions.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | Stanford University NIH-funded |
| Lab location | 1 site (Stanford, United States) |
| Project ID | NIH-11311896 on NIH RePORTER |
What this research studies
This project examines how smooth muscle cells in artery walls change during atherosclerosis by combining human genetic studies, single-cell maps of diseased vessels, and mouse experiments. The team will identify DNA regulatory switches (enhancers) and key transcription factors that push cells toward two harmful end states: fibromyocytes that make scar-like tissue and chondromyocytes that promote calcification. They will link coronary artery disease genetic risk variants to specific enhancers and transcription factors using multi-omic single-cell data and targeted mouse genetic models. The goal is to trace the cell paths and pinpoint molecular switches that could be targeted to prevent artery clogging.
Who could benefit from this research
Good fit: Adults with coronary artery disease, atherosclerosis, or high cardiovascular risk are the people most likely to be relevant to this work and to participate in related studies in the future.
Not a fit: People without cardiovascular disease or those seeking immediate treatment options are unlikely to get direct or immediate benefit from this basic science research.
Why it matters
Potential benefit: If successful, this work could reveal new molecular targets to prevent harmful artery wall cell changes that lead to blocked arteries, heart attacks, and strokes.
How similar studies have performed: Earlier human genetics and single-cell studies have shown smooth muscle cell transitions in atherosclerosis and mouse models have modified disease by changing certain genes, but comprehensively mapping the regulatory networks is novel and ongoing.
Where this research is happening
Stanford, United States
- Stanford University — Stanford, United States (Active)
Researchers
- Principal investigator: Quertermous, Thomas — Stanford University
- Study coordinator: Quertermous, Thomas
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.