John Varga
University of Michigan, MI·Medicine & Clinical Research
In systemic sclerosis (SSc), also called scleroderma, the body lays down too much scar-like connective tissue, a process called fibrosis. The scarring stiffens the skin and permanently damages internal organs, and it can be deadly.
- Fields
Medicine & Clinical Research
Biochemistry
Microbiology & Immunology
- Topics
systemic sclerosis
SSc
scleroderma
- Grants
- 1 known grant, through Aug 2028
What they work on
- Map where CD38, an immune-cell enzyme that breaks down the energy molecule NAD, is expressed in systemic sclerosis patient biopsies, and determine its cell type-specific role in fibrosis using engineered mice and disease models.
- Map NNMT, a fibroblast enzyme that links metabolism to DNA methylation changes, in SSc biopsies, and define its cell type-specific role in driving scarring using mouse models and drug inhibitors.
- Test how CD38 and NNMT interact, specifically whether NAM produced by CD38 fuels NNMT activity and reprograms fibroblasts toward fibrosis.
More about the research
Why fibrosis keeps going in SSc is poorly understood, and no treatment works well. This project asks whether a shift in how cells handle a central energy molecule, nicotinamide adenine dinucleotide (NAD), drives the scarring, and whether that shift could be a target for new drugs.
Why it matters
Systemic sclerosis causes organ scarring that can be fatal, and patients currently have no effective treatment for fibrosis. By clarifying how CD38 and NNMT disturb NAD metabolism in SSc, this work could point to new drug targets. Treatments aimed at these targets might reduce disease severity or delay its deadly complications.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Mengqi Huang
University of Pittsburgh, PA·Medicine & Clinical Research·Early-career
Identify the DNA control regions (cis-regulatory elements) that regulate the TGF-β3 gene in skin fibroblasts from patients with systemic sclerosis.
Karthikeyani Chellappa
Brown University, RI·Biochemistry
Define how nicotinamide (NAM), the main NAD building block, crosses the plasma membrane of mammalian cells through the biphasic transport system the lab discovered.
Shervin Assassi
University of Texas Health Science Center at Houston, TX·Medicine & Clinical Research
Determine how much removing Irf7 specifically from fibroblasts reduces skin fibrosis, in bleomycin-induced and Tsk1 mouse models of dermal fibrosis.
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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