Zhongkui Hong
Texas Tech University, TX·Biomedical Engineering
Atherosclerosis, the buildup of plaque in artery walls, is the leading cause of heart attacks and strokes. A key early step is when vascular smooth muscle cells (VSMCs), the muscle cells in blood vessel walls, move from the middle layer of the artery into the inner lining.
- Fields
Biomedical Engineering
Physiology
Pharmacology
- Topics
atherosclerosis
cardiovascular disease
vascular smooth muscle cells
- Grants
- 1 known grant, through Apr 2029
What they work on
- 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.
- Determine how IAG933, a first-in-class TEAD inhibitor that blocks YAP/TAZ signaling, selectively strengthens adhesion to collagen (COL1) and elastin (ELN) while limiting fibronectin-driven migration.
- Test whether IAG933 prevents early plaque formation and slows established atherosclerosis in ApoE⁻/⁻ mice.
More about the research
Their movement depends on how they grip the extracellular matrix (ECM), the protein scaffold around cells, and on how stiff that scaffold is.
Why it matters
Atherosclerosis underlies most heart attacks and strokes. If IAG933 restores healthy smooth muscle cell adhesion and blocks harmful migration, it could become a new way to prevent or slow plaque formation. This would offer a therapy that targets how vessel cells sense their surroundings, not only cholesterol levels. People at risk of cardiovascular disease could eventually benefit.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Guizhen Zhao
University of Houston, TX·Physiology
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.
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.
Jennifer Chen
University of California-San Francisco, CA·Medicine & Clinical Research
Determine how ceramide inhibits YAP/TAZ, signaling proteins of the Hippo growth-control pathway, in hepatic stellate cells, using gain- and loss-of-function experiments and mice lacking acid ceramidase in these cells.
The school
Texas Tech University: 9 labs on PI Pages, $257M a year on research, 415 research doctorates a year.
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