Ying Chen
Washington University in St Louis, MO·Medicine & Clinical Research
Some forms of chronic kidney disease are inherited. One of the most common is autosomal dominant tubulointerstitial kidney disease caused by mutations in the uromodulin gene (ADTKD-UMOD).
- Fields
Medicine & Clinical Research
Physiology
Biology
- Topics
chronic kidney disease
autosomal dominant tubulointerstitial kidney disease
uromodulin
- Grants
- 1 known grant, through Aug 2029
What they work on
- 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.
- Develop MANF-based therapies and test whether restoring autophagy reduces fibrosis and improves kidney function in a CRISPR/Cas9 mouse model carrying the most common human UMOD mutation.
- Define the role of neuroplastin, a newly identified receptor for MANF, in autophagy, tubular cell death and disease progression in ADTKD-UMOD.
More about the research
Uromodulin (UMOD) is a protein made mostly by cells lining the thick ascending limb (TAL), a segment of the kidney's tubules. In this disease, mutant UMOD misfolds and builds up inside these cells. The kidney then scars, a process called fibrosis, and gradually loses function. There is no targeted therapy, and this project aims to develop one.
Why it matters
ADTKD-UMOD is a leading inherited kidney disease with no targeted treatment, and it progresses to kidney failure. By developing autophagy activators that target MANF and its receptor, this work could lead to mechanism-based therapies that slow kidney scarring and preserve kidney function in patients with uromodulin mutations.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
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.
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.
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
Washington University in St Louis: 97 labs on PI Pages, $1.2B a year on research, 365 research doctorates a year.
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