Yanlin Wang
University of Connecticut, CT·Medicine & Clinical Research
Chronic kidney disease affects more than 37 million Americans, and once kidneys begin to scar there is little that reliably stops the decline. Two processes drive that decline together: inflammation, in which immune cells pile into kidney tissue and release signals that damage it, and fibrosis, the stiff scar tissue that accumulates as the end result of chronic inflammation.
- Fields
Medicine & Clinical Research
Physiology
Microbiology & Immunology
- Topics
chronic kidney disease
kidney fibrosis
renal inflammation
- Grants
- 1 known grant, through Dec 2026
What they work on
- Determine the role of PU.1, a transcription factor that switches on genes in immune cells, in macrophage activation and polarization, using cultured macrophages and mouse models of kidney injury.
- Dissect the molecular mechanisms by which PU.1 promotes macrophage activation, testing whether it acts by inducing NLRP3 inflammasome expression and assembly, the protein complex that releases inflammatory messengers.
- Test whether a selective PU.1 inhibitor suppresses inflammatory and scar-promoting molecules and reduces kidney fibrosis, evaluating its therapeutic potential in experimental chronic kidney disease.
- Compare PU.1 levels and inflammatory signatures in experimental kidney disease models with human kidney tissue from patients with chronic kidney disease.
More about the research
Central to the inflammatory side are macrophages, immune cells that switch into an activated, damaging state. What flips that switch is still not fully mapped, and this project aims to find out, with the goal of designing treatments that interrupt it.
Why it matters
Treatment options for chronic kidney disease are limited, and patients often progress toward kidney failure. Identifying PU.1 and the NLRP3 inflammasome as the switch that turns macrophages into drivers of kidney inflammation and scarring could provide a drug target; the selective PU.1 inhibitor tested here may point toward therapies that slow fibrosis in the millions of people living with chronic kidney disease.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Stephanie Mutchler
University of Pittsburgh, PA·Physiology·Early-career
Determine how aldosterone and the mineralocorticoid receptor regulate Piezo1 levels and activity in the distal nephron, using tdTomato-tagged Piezo1 mice, RNAscope, immunostaining and calcium and current recordings from isolated collecting ducts.
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.
Jacqueline Ho
University of Pittsburgh, PA·Medicine & Clinical Research
Test whether turning on the miR-17~92 microRNA cluster in adult kidney tubule lining cells is enough to protect mice against kidney fibrosis, using genetically engineered mice in which the cluster can be switched on.
The school
University of Connecticut: 31 labs on PI Pages, $434M a year on research, 360 research doctorates a year.
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