Guizhen Zhao
University of Houston, TX·Physiology
Atherosclerosis, the buildup of fatty plaques in artery walls, underlies the cardiovascular diseases that are the leading cause of death worldwide. Current drugs mostly manage risk factors rather than the cells that build plaques, and substantial risk remains.
- Fields
Physiology
Pharmacology
Biochemistry
- Topics
atherosclerosis
cardiovascular disease
metaboloepigenetics
- Grants
- 1 known grant, through Feb 2029
What they work on
- Define whether the BAF60c–PPARγ axis protects against atherosclerosis, using male and female mice with smooth-muscle-specific knockout or transgenic overexpression of BAF60c, a chromatin-remodeling subunit.
- Determine how BAF60c loss disturbs PPARγ, a metabolic regulator, and drives smooth muscle dysfunction, including excess glycolysis, oxidative stress, lipid buildup and conversion to foam cells, in cultured vascular smooth muscle cells.
- Examine how BAF60c links the SWI/SNF chromatin remodeling complex to transcription factors such as SRF and PPARγ to keep vascular smooth muscle cells in their healthy contractile state.
More about the research
Two early events in disease are changes in metabolism and changes in epigenetics, the chemical and structural packaging that controls which genes are accessible. These two processes interact, an idea called "metaboloepigenetics." How this interplay reshapes the cells of the artery wall during atherosclerosis is not known.
Why it matters
Atherosclerosis-related heart disease remains the leading cause of death in the U.S., and current therapies leave substantial residual risk. Defining how BAF60c and PPARγ protect artery smooth muscle cells could point to new treatment targets. One possibility is combining metabolism inhibitors with epigenetic drugs that act directly on plaque-forming cells.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
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.
Zhongkui Hong
Texas Tech University, TX·Biomedical Engineering
Define how stiffness and composition of the extracellular matrix control adhesion and migration of vascular smooth muscle cells through YAP/TAZ mechanotransduction, using cells from ApoE⁻/⁻ mice.
Yujun Cai
Yale University, CT·Pharmacology
Investigate how PDE10A drives vascular smooth muscle cells exposed to high phosphate to turn into bone-like cells and calcify, using PDE10A knockdown and inhibition in cultured cells and PDE10A-deficient animals.
The school
University of Houston: 21 labs on PI Pages, $239M a year on research, 374 research doctorates a year.
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