Jacqueline Ho
University of Pittsburgh, PA·Medicine & Clinical Research
About 37 million people in the United States, roughly 15% of the population, have chronic kidney disease (CKD). No treatment specifically stops it from getting worse, and it can lead to kidney failure, dialysis or transplant.
- Fields
Medicine & Clinical Research
Genetics
Physiology
- Topics
chronic kidney disease
renal fibrosis
kidney fibrosis
- Grants
- 1 known grant, through May 2027
What they work on
- 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.
- Determine how losing miR-17~92 in adult kidney lining cells increases fibrosis in mice, using mouse strains in which the cluster can be removed on demand.
- Define how miR-17~92 in kidney lining cells controls scar-promoting factors that pass signals to the surrounding tissue during progression to chronic kidney disease.
More about the research
Whatever the original cause, advancing CKD ends in scarring of the kidney, called fibrosis. Fibrosis is normally part of healing. When it goes wrong, the kidney piles up extracellular matrix (ECM), the protein scaffold between cells, made mainly of collagen. Learning what drives this early buildup could point to new treatments.
Why it matters
Chronic kidney disease affects about 37 million Americans, and current therapies at most delay its progress toward kidney failure. If miR-17~92 limits kidney scarring, members of this microRNA family or the genes they control could become the basis of a new treatment approach. Such a treatment could slow fibrosis in people with CKD.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Ying Chen
Washington University in St Louis, MO·Medicine & Clinical Research
Determine the molecular mechanisms by which MANF, an ER protein, activates autophagy and mitophagy to clear toxic mutant uromodulin and limit STING-driven inflammation in kidney thick ascending limb cells.
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.
Yanlin Wang
University of Connecticut, CT·Medicine & Clinical Research
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.
The school
University of Pittsburgh: 83 labs on PI Pages, $1.5B a year on research, 403 research doctorates a year.
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