Rujun Gong
University of Toledo, OH·Medicine & Clinical Research
Diabetes is the leading cause of kidney failure, and there is still no definitive treatment for diabetic kidney disease (DKD). A key early event is damage to podocytes.
- Fields
Medicine & Clinical Research
Physiology
Pharmacology
- Topics
diabetic kidney disease
diabetic nephropathy
GSK3β
- Grants
- 1 known grant, through May 2027
What they work on
- 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.
- Determine the role of podocyte GSK3β in diabetic nephropathy by making it overactive or deleting it only in podocytes. Use streptozotocin-treated type 1 diabetic mice with one kidney removed and db/db type 2 diabetic mice.
- Test whether the GSK3β-blocking drugs microdose lithium and tideglusib can rescue already-established diabetic kidney disease in mice.
- Test whether GSK3β inhibition works with retinoic acid and its receptor RARα, a podocyte repair switch, to protect the kidney. Use mice lacking both genes in podocytes and combined drug treatment.
More about the research
These are specialized cells that wrap around the kidney's tiny blood filters and keep protein in the blood. In diabetes, podocytes respond poorly to insulin, suffer oxidative damage and age prematurely (senescence), which leads to kidney decline. This project focuses on one enzyme that may tie these problems together.
Why it matters
Diabetic kidney disease affects hundreds of millions of people and is the leading cause of kidney failure, with no definitive treatment. If blocking GSK3β protects podocytes, existing or new drugs that inhibit this enzyme, such as low-dose lithium or tideglusib, possibly combined with retinoic acid, could be tested in clinical trials to slow kidney damage in people with diabetes.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Sandeep Mallipattu
Stony Brook University, NY·Medicine & Clinical Research
Determine whether N-glycosylated apolipoprotein J (ApoJ), a protein released by kidney filter cells, protects the kidney in diabetic kidney disease, building on mice expressing human KLF6 in podocytes that showed less tubule injury and fibrosis.
Jeffrey Schelling
Case Western Reserve University, OH·Medicine & Clinical Research
Determine whether FATP2, a fatty acid transporter in the kidney's proximal tubule, drives fat-induced cell death and progression of diabetic kidney disease, using mouse models.
Yi Tan
University of Arizona, AZ·Pharmacology
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.
The school
University of Toledo: 10 labs on PI Pages, $73M a year on research, 120 research doctorates a year.
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