Yi Tan
University of Arizona, AZ·Pharmacology
Diabetes and high cholesterol damage the heart and blood vessels, yet treatments that prevent that damage remain limited or carry side effects. These two projects ask whether fibroblast growth factors (FGFs), natural signaling proteins that regulate cell growth and metabolism, can be redesigned to protect the cardiovascular system.
- Fields
Pharmacology
Physiology
Medicine & Clinical Research
- Topics
diabetic cardiomyopathy
type 2 diabetes
atherosclerosis
- Grants
- 2 known grants, through Mar 2030
What they work on
- Optimize doses of the stabilized FGF16 variant rhFGF16delta33 that protect against diabetic cardiomyopathy in two type 2 diabetic mouse models, high-fat diet/streptozotocin mice and db/db mice.
- Test whether FGF16 protects the diabetic heart by acting directly on cardiomyocytes, using cardiomyocyte-specific FGF16 deletion along with measures of hypertrophy, inflammation and fibrosis.
- Test whether FGF16 signals through the receptors FGFR1/2 to activate AMPK, an energy-sensing enzyme, and thereby boost fatty acid oxidation and mitochondrial oxidative phosphorylation in heart muscle cells.
- Determine the role of endogenous FGF1 in atherosclerosis and optimize doses of the non-mitogenic variant FGF1ΔHBS in two atherogenic mouse models, including ApoE-knockout mice.
- Determine whether FGF1ΔHBS lowers cholesterol by inhibiting cholesterol biosynthesis in hepatocytes and suppressing dietary and biliary cholesterol absorption in intestinal enterocytes, and define the mechanisms in each tissue.
More about the research
In both cases the lab works with an engineered FGF variant with improved properties and tests it in mouse models, asking how it acts at the level of organs, cells and signaling pathways.
Why it matters
People with type 2 diabetes face heart damage that current therapies do not reliably prevent, and people at risk of atherosclerosis rely on cholesterol-lowering drugs such as statins that carry side effects. Engineered growth-factor variants, the stabilized rhFGF16delta33 and the non-mitogenic FGF1ΔHBS, may offer more specific ways to prevent these conditions. These mouse studies aim to provide the mechanistic groundwork for future clinical testing.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Rujun Gong
University of Toledo, OH·Medicine & Clinical Research
Define how GSK3β, an enzyme that relays insulin signals, damages podocytes in diabetic conditions. Test its effects on insulin signaling, the Nrf2 antioxidant response, and senescence through p53 and p16INK4A in cultured podocytes.
Dongmin Liu
Virginia Polytechnic Institute and State University, VA·Pharmacology
Characterize the anti-diabetic and anti-obesity effects of daily oral elenolic acid in diet-induced obese and db/db diabetic mice, using metabolic profiling and euglycemic-hyperinsulinemic clamps to measure insulin sensitivity.
Jun Yoshioka
CUNY City College, NY·Physiology
Test whether Arrdc4, an adaptor protein switched on by high glucose, is controlled by the cell's glucose-sensing gene machinery, linking high blood sugar to ER stress in cardiomyocytes.
The school
University of Arizona: 36 labs on PI Pages, $1.0B a year on research, 487 research doctorates a year.
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