Jeffrey Schelling
Case Western Reserve University, OH·Medicine & Clinical Research
Diabetes is a leading cause of kidney failure. Almost half of new cases of end-stage kidney disease in the US stem from diabetic kidney disease (DKD).
- Fields
Medicine & Clinical Research
Physiology
Biochemistry
- Topics
diabetic kidney disease
chronic kidney disease
end-stage renal disease
- Grants
- 1 known grant, through Jun 2027
What they work on
- 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.
- Define how Plin5, a protein that builds fat-storage droplets linked to mitochondria, shapes proximal tubule metabolism and protects cells in diabetic kidney disease.
- Test the therapeutic value of blocking FATP2 for preserving kidney function and reducing tubular atrophy in diabetic kidney disease.
More about the research
Doctors often track damage to the kidney's filters, the glomeruli. Yet shrinkage and loss of the kidney's tubules, called tubular atrophy, better predicts how fast DKD gets worse. Why tubule cells die is not known.
Why it matters
More than 600,000 people in the US need dialysis or a transplant because of kidney failure, and diabetic kidney disease is a major cause. Pinpointing how fat uptake through FATP2 kills tubule cells, and how Plin5 protects them, could identify drug targets such as FATP2 inhibitors to slow kidney disease.
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.
Mon-Wei Yu
Icahn School of Medicine at Mount Sinai, NY·Medicine & Clinical Research·Early-career
Determine whether C5a–C5aR1 signaling in renal tubular epithelial cells, the cells lining kidney tubules, drives cellular senescence and kidney fibrosis after injury, using mouse models.
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.
The school
Case Western Reserve University: 34 labs on PI Pages, $643M a year on research, 213 research doctorates a year.
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