Sandeep Mallipattu
Stony Brook University, NY·Medicine & Clinical Research
Diabetes is the leading path to kidney failure, and even with good blood sugar control and current drugs a large share of patients still progress to end-stage kidney disease and dialysis. The kidney filters blood through millions of tiny units; specialized cells called podocytes form the filter itself, while proximal tubule cells downstream reclaim useful material from the filtrate.
- Fields
Medicine & Clinical Research
Physiology
Biochemistry
- Topics
diabetic kidney disease
end-stage kidney disease
podocyte
- Grants
- 1 known grant, through Feb 2029
What they work on
- 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.
- Define how ApoJ primes CaMK1D signaling in proximal tubule cells, following its uptake through the receptor LRP2 and its binding to calmodulin to activate the CaMKK-CaMK1D pathway under diabetic conditions.
- Establish how activation of CaMK1D, a calcium/calmodulin-dependent kinase, preconditions proximal tubule cells against injury, testing protection of mitochondria and cell survival under high glucose with genetic and pharmacological Camk1d inhibition.
- Map which tubule cells respond to podocyte signals using single-nuclei RNA sequencing and single-nuclei ATAC sequencing, and identify the secreted proteins involved by tandem mass spectrometry of the podocyte secretome.
More about the research
Podocyte loss starts the damage in diabetic kidney disease, but how badly the proximal tubule is injured is what best predicts whether a patient's disease will progress. This project asks whether the filter cells send chemical signals that protect the tubule, and whether that conversation can be harnessed to slow the disease.
Why it matters
Many people with diabetic kidney disease still progress to end-stage kidney disease despite glycemic control, renin-angiotensin blockade, and SGLT2 inhibitors. Because proximal tubule injury drives that progression, a protective signal sent from podocytes to the tubule could become a therapeutic target for patients whose kidney disease is advancing rapidly, and urinary ApoJ, already raised in early disease, may be informative as a marker.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
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.
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.
Jeffrey Beamish
University of Michigan, MI·Medicine & Clinical Research
Define the genes that the transcription factor Pax8 controls in kidney proximal tubule cells before and after ischemic injury, using new in vivo and in vitro models of normal and regenerating epithelium.
The school
Stony Brook University: 32 labs on PI Pages, $319M a year on research, 289 research doctorates a year.
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