Kurt Zimmerman
University of Oklahoma-Health Sciences Center, OK·Microbiology & Immunology
Polycystic kidney disease fills the kidneys with fluid-filled sacs (cysts) that slowly destroy kidney function over decades, and only one drug exists for its most common inherited form despite years of research. Two linked problems stand in the way of new treatments.
- Fields
Microbiology & Immunology
Medicine & Clinical Research
Genetics
- Topics
polycystic kidney disease
kidney cysts
kidney resident macrophages
- Grants
- 3 known grants, through Jun 2030
What they work on
- Generate single-cell RNA sequencing data from the inducible Pax8 rtTA tetocre Pkd1f/f mouse model and merge it with the lab's existing mouse polycystic kidney disease atlas, analyzing it with the team's deep learning model.
- Compare molecular signatures across mouse models and ADPKD patients to predict which models best match human disease, and test whether signaling networks within and between cells are conserved across species.
- Build a user-friendly web portal that lets researchers search the cross-model atlas for genes of interest in mouse models of cystic kidney disease.
- Track how blood monocytes refill the kidney resident macrophage niche after temporary depletion, using monocyte fate-mapping mice in both normal and cystic mice.
- Identify genes required for niche refilling and test whether targeting Cx3cr1, a monocyte receptor, delays refilling and slows cyst growth in mice.
More about the research
First, scientists study the disease in many different mouse models that may not match patients. Second, immune cells living in the kidney appear to speed cyst growth, but they cannot yet be safely targeted. The lab's projects tackle both problems, and it also runs a shared immunology and data-analysis core.
Why it matters
Patients with polycystic kidney disease have very few drug options. A cross-species atlas could help researchers pick the mouse models that best predict patient responses and reveal new signaling targets, making preclinical drug testing more useful. A kidney-specific way to deplete harmful resident macrophages could lead to treatments that slow cyst growth without weakening immunity elsewhere. It may also help with acute kidney injury and chronic kidney disease.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
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.
Timothy Blackwell
University of Michigan, MI·Medicine & Clinical Research
Detect gene activity biomarkers of pre-clinical disease in asymptomatic relatives of familial pulmonary fibrosis patients, using single-cell RNA sequencing of blood immune cells such as CD14+ monocytes alongside high-resolution CT findings.
Kyle Hewitt
University of Nebraska Medical Center, NE·Genetics
Define how Samd14, a gene switched on during anemia, supports c-Kit signaling and survival of red blood cell precursors, using primary human and mouse cells.
The school
University of Oklahoma-Health Sciences Center: 11 labs on PI Pages, $474M a year on research, 31 research doctorates a year.
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