Clint Miller
University of Virginia, VA·Genetics
Coronary artery disease (CAD) is the narrowing of the arteries that supply the heart. It remains a major global health burden despite treatments that target risk factors.
- Fields
Genetics
Medicine & Clinical Research
Physiology
- Topics
coronary artery disease
atherosclerosis
myocardial infarction
- Grants
- 2 known grants, through Jun 2028
What they work on
- Determine how FHL5, a helper protein that tunes gene activity, causes vascular dysfunction through the actin cytoskeleton, the extracellular matrix and vessel constriction. The work will use human vascular cells and arteries studied ex vivo.
- Map where FHL5 binds DNA and which proteins it interacts with. Use these data to build multi-omic gene regulatory networks linking the FHL5 regulome to subclinical and advanced vascular disease.
- Apply multimodal single-cell profiling to early and advanced diseased coronary segments from an ancestrally diverse biobank. The aim is to map QTLs, DNA variants that change gene activity, and the regulatory mechanisms in each smooth muscle cell state.
- Validate and discover candidate causal CAD genes and regulatory elements using perturbation assays coupled with high-throughput phenotyping of coronary artery smooth muscle cells.
- Place disease-stage and cell-state markers in context with spatial imaging of intact coronary tissue. Link the results to population genetics, clinical imaging and cardiometabolic biobanks.
More about the research
Genome-wide association studies (GWAS) scan the DNA of many people for variants linked to disease. They have tied more than 300 regions of the genome to CAD risk, yet the causal genes and mechanisms behind most of them remain unknown. More than half of the CAD and heart attack regions act independently of classical risk factors and may point to problems in the vessel wall itself.
Why it matters
CAD, heart attack and coronary artery calcification place a heavy public health burden on populations worldwide. This work aims to pin down which genes and regulatory switches in the artery wall drive these conditions. It could reveal biomarkers and new targets for therapies that act on the vessel wall itself. Disease-stage-specific markers may improve risk prediction, and the findings could inform early treatment or prevention strategies.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Daniel Li
Stanford University, CA·Genetics·Early-career
Determine how losing ZEB1, a transcription factor linked to coronary artery disease risk, changes gene activity, epigenetic state and plaque features in smooth muscle–derived cells, using a Zeb1 knockout mouse model of atherosclerosis.
Robert Wirka
University of North Carolina at Chapel Hill, NC·Genetics
Track individual smooth muscle cells as they multiply and choose fates during atherosclerosis, using a barcoding mouse model compatible with single-cell RNA sequencing, with and without Twist1 knockout.
Joseph Miano
Augusta University, GA·Physiology
Define the coronary artery disease that develops in mice lacking Lmod1 only in vascular smooth muscle cells, using mouse genetics, spatial gene-activity profiling and immuno-electron microscopy of artery tissue.
The school
University of Virginia: 43 labs on PI Pages, $814M a year on research, 413 research doctorates a year.
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