Yujun Cai
Yale University, CT·Pharmacology
Arteries can gradually stiffen with bone-like deposits as calcium crystals build up in their walls. This arterial calcification is common in people with chronic kidney disease (CKD) and diabetes.
- Fields
Pharmacology
Medicine & Clinical Research
Physiology
- Topics
vascular calcification
arterial calcification
medial artery calcification
- Grants
- 1 known grant, through May 2027
What they work on
- 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.
- Examine the therapeutic potential of PDE10A inhibition by testing whether blocking the enzyme reduces arterial calcification, as a possible treatment for patients with chronic kidney disease and peripheral artery disease.
- Assess whether PDE10A promotes calcification by activating p38 MAPK, a signaling protein, which in turn raises MMP-3 (stromelysin-1), an enzyme that degrades the material around cells in the artery wall.
More about the research
It is also common in peripheral artery disease (PAD), in which narrowed arteries reduce blood flow to the legs. Calcification in the middle muscle layer of the artery is strongly linked to cardiovascular illness and death, yet no usable drugs exist to prevent or treat it.
Why it matters
Patients with diabetes, chronic kidney disease and peripheral artery disease often develop calcified leg arteries, which raise their risk of cardiovascular illness, death and amputation. No drugs currently prevent or treat this calcification. This work aims to establish PDE10A as a new drug target. Blocking it could become a strategy to reduce medial artery calcification and help prevent amputations in these patients.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Albert Sinusas
Yale University, CT·Medicine & Clinical Research
Develop a multimodality imaging approach that uses early bright regions on non-contrast CT to guide hydrogel injection through the chest wall into injured heart muscle, in a pig model of reperfused heart attack.
Dogukan Mizrak
University of Michigan, MI·Medicine & Clinical Research
Define the molecular triggers and downstream effects of CART signaling in human aortic smooth muscle cells in vitro, testing whether it drives wall remodeling and medial calcification, mineral buildup that stiffens the artery.
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.
The school
Yale University: 73 labs on PI Pages, $1.5B a year on research, 438 research doctorates a year.
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