Kirk Campbell
University of Pennsylvania, PA·Physiology
The kidney filters blood through roughly a million tiny units called glomeruli. Wrapped around each filter are podocytes, octopus-shaped cells whose extensions form the final barrier that keeps protein in the blood.
- Fields
Physiology
Pharmacology
Medicine & Clinical Research
- Topics
podocyte
glomerular disease
proteinuria
- Grants
- 1 known grant, through May 2029
What they work on
- Define how Hippo-YAP signaling regulates the calcium-activated potassium channel KCa3.1 in podocytes, including whether nuclear YAP protects the actin cytoskeleton by repressing the KCNN4 gene that encodes it.
- Determine how calcium-activated potassium channel activity injures podocytes, tracing the link between potassium efflux, pathogenic intracellular calcium signaling and focal adhesion and cytoskeletal disruption.
- Test the in vivo interaction and functional consequence of YAP inhibition of KCNN4/KCa3.1 using animal models of glomerular disease.
- Optimize KCa3.1 inhibitors by rational design and medicinal chemistry and test whether they protect podocytes, reduce albuminuria and slow kidney disease progression in in vivo glomerular disease models.
More about the research
When podocytes are injured, protein leaks into the urine and kidney function declines, a pattern seen in diseases such as focal segmental glomerulosclerosis (FSGS). Few drugs target this process, largely because the signaling pathways that keep podocytes alive and structurally intact are poorly mapped. This project follows one such pathway toward a possible treatment.
Why it matters
Proteinuric kidney diseases such as FSGS and other podocytopathies progress toward kidney failure with few targeted therapies available, and no KCa3.1 inhibitors are currently in clinical development for them. By defining how Hippo-YAP signaling controls this potassium channel in podocytes and optimizing inhibitors that reduce protein in the urine in animal models, the work could provide a new therapeutic strategy for patients with progressive glomerular disease.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Sethu Madhavan
Ohio State University, OH·Medicine & Clinical Research
Define how ACOX1, the rate-limiting enzyme of peroxisomal fat breakdown, drives injury specific to the APOL1 G1 and G2 kidney risk variants, using overexpression plus gain- and loss-of-function manipulation in human podocytes.
Daniel Brennan
Johns Hopkins University, MD·Medicine & Clinical Research
Determine how donor APOL1 genotype affects time to graft failure, kidney function decline, acute rejection and proteinuria in recipients of kidneys from African American donors.
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.
The school
University of Pennsylvania: 90 labs on PI Pages, $2.2B a year on research, 750 research doctorates a year.
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