Mon-Wei Yu
Icahn School of Medicine at Mount Sinai, NY·Medicine & Clinical Research·Early-career
Chronic kidney disease (CKD), a slow and lasting loss of kidney function, is a major cause of illness and death worldwide. People who suffer repeated episodes of acute kidney injury (AKI), a sudden drop in kidney function, are more likely to develop CKD.
- Fields
Medicine & Clinical Research
Microbiology & Immunology
Physiology
- Topics
chronic kidney disease
acute kidney injury
AKI-to-CKD transition
- Grants
- 1 known grant, through May 2028
What they work on
- 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.
- Test whether C5aR1 activation in kidney resident macrophages and other myeloid immune cells protects the kidney during the acute phase of acute kidney injury, using mouse models and immunological approaches.
- Clarify how C5aR1 activity in different kidney cell types shapes the transition from acute kidney injury to chronic kidney disease, to inform the potential use of complement-regulating therapies.
More about the research
Despite new biomarkers and greater awareness of kidney health, CKD and end-stage kidney disease keep rising, and no treatment stops the progression from acute injury to chronic disease.
Why it matters
Patients who survive acute kidney injury often go on to develop chronic kidney disease, and no current therapy stops that progression. By showing where C5aR1 signaling helps and where it harms, this work could lay groundwork for complement-regulating therapies. Such drugs might one day be targeted to protect injured kidneys from long-term scarring and failure.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
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 Beamish
University of Michigan, MI·Medicine & Clinical Research
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.
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
Icahn School of Medicine at Mount Sinai: 45 labs on PI Pages, $1.0B a year on research, 62 research doctorates a year.
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