Mengqi Huang
University of Pittsburgh, PA·Medicine & Clinical Research·Early-career
Systemic sclerosis (SSc), also called scleroderma, is an autoimmune disease that causes fibrosis, the stiff scarring of skin and internal organs. The main cells that cause this scarring are myofibroblasts, activated cells that lay down excess tissue.
- Fields
Medicine & Clinical Research
Genetics
Microbiology & Immunology
- Topics
systemic sclerosis
SSc
scleroderma
- Grants
- 1 known grant, through Apr 2030
What they work on
- Identify the DNA control regions (cis-regulatory elements) that regulate the TGF-β3 gene in skin fibroblasts from patients with systemic sclerosis.
- Find whether FRA-2/FOSL2 or other upstream factors switch on TGF-β3 in patient skin fibroblasts, by combining single-cell gene-activity and epigenetic profiles.
- Assess how strongly TGF-β3 drives organ fibrosis and myofibroblast formation in mouse models of systemic sclerosis.
More about the research
No treatments currently target them. TGF-β3 is a signaling protein in the TGF-β family, which drives myofibroblast formation. Higher TGF-β3 levels track with the severity of skin fibrosis, and blocking TGF-β3 reduced lung fibrosis in a mouse model. What makes these cells produce so much TGF-β3 is unknown. This project asks how that switch is controlled.
Why it matters
People with systemic sclerosis currently have no treatments that target the myofibroblasts driving skin and organ scarring. Identifying what controls TGF-β3 production in these cells could reveal more specific drug targets within the TGF-β pathway. This may make SSc treatment safer and more effective than broadly blocking TGF-β.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
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.
John Varga
University of Michigan, MI·Medicine & Clinical Research
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.
Sandeep Agarwal
Baylor College of Medicine, TX·Medicine & Clinical Research
Determine whether cadherin-11 is needed in macrophages, type II alveolar epithelial cells or fibroblasts for macrophage recruitment and lung fibrosis, using mice with cell-specific Cdh11 deletion plus transcriptomic profiling.
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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