Daniel Li
Stanford University, CA·Genetics·Early-career
Coronary artery disease (CAD), the narrowing of the arteries that feed the heart, is the leading cause of death worldwide. Beyond lowering cholesterol and other blood fats, there are few treatments.
- Fields
Genetics
Medicine & Clinical Research
Biology
- Topics
coronary artery disease
atherosclerosis
vascular smooth muscle cells
- Grants
- 1 known grant, through Aug 2030
What they work on
- 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.
- Test whether ZEB1 counterbalances its relative ZEB2 to keep smooth muscle cells in a mature state, using functional genomics and proteomics to compare the epigenetic partner proteins each factor recruits.
- Define how ZEB factors interact with other coronary artery disease–associated genes, using single-cell genomics in animal and human models to connect genetic risk to smooth muscle cell transitions.
More about the research
A key reason is that scientists cannot yet connect inherited risk genes to the processes that actually cause disease. Smooth muscle cells (SMCs), the cells that form the muscular wall of blood vessels, are central here. During atherosclerosis, the build-up of fatty plaques in artery walls, SMCs lose their mature identity and migrate out of the vessel wall to help form a fibrous cap over the plaque. SMCs are also the main cell type carrying genetic susceptibility to CAD.
Why it matters
Most coronary artery disease treatments target cholesterol, leaving a gap in options. By showing how the CAD risk genes ZEB1 and ZEB2 control smooth muscle cell behavior in artery walls, this work could support better tools for predicting a person's risk and point to precision therapies. Such advances may help prevent heart attacks.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
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.
Clint Miller
University of Virginia, VA·Genetics
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.
The school
Stanford University: 87 labs on PI Pages, $1.6B a year on research, 739 research doctorates a year.
Reach out
A start for your email. Fill in the brackets.