Jeffrey Beamish
University of Michigan, MI·Medicine & Clinical Research
When kidneys lose blood flow, the cells lining their tiny tubes can be badly damaged, causing acute kidney injury (AKI). AKI is common and costly, it has no available treatments, and it can lead to chronic kidney disease (CKD).
- Fields
Medicine & Clinical Research
Genetics
Physiology
- Topics
acute kidney injury
chronic kidney disease
Pax8
- Grants
- 1 known grant, through Dec 2030
What they work on
- 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.
- Identify gene regulatory networks that Pax8 controls together with other proximal tubule transcription factors at enhancers, DNA switch regions that show altered chromatin modifications after injury.
- Identify how ischemic stress changes Pax8 function, testing whether Pax8 acts as a switch between a resilient, de-differentiated cell state and a mature, functional one.
More about the research
Surviving cells can rebuild the damaged tubes, but recovery varies widely between patients. Some regenerating cells return to normal, while others get stuck in a failed repair state that leads to CKD. What decides which path a cell takes?
Why it matters
Acute kidney injury affects many patients, has no available treatments, and can progress to chronic kidney disease. Learning how Pax8 guides kidney cells toward successful repair or failed repair could reveal new treatment targets for AKI. It could also help with other diseases where the lining cells of organs lose their normal function.
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.
Dong Zhou
University of Connecticut, CT·Physiology
Determine the mechanistic role of extracellular matrix protein 1 (ECM1), a secreted matrix protein switched on within hours of injury, in forming the kidney microenvironment after acute kidney injury, using ex vivo approaches.
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.
The school
University of Michigan: 124 labs on PI Pages, $2.1B a year on research, 963 research doctorates a year.
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