Yong Huang
University of Virginia, VA·Medicine & Clinical Research
Idiopathic pulmonary fibrosis (IPF) is an age-linked disease in which scar tissue gradually builds up in the lungs and makes breathing harder. The scarring is worst at the outer edges and lower parts of the lungs.
- Fields
Medicine & Clinical Research
Physiology
Biomedical Engineering
- Topics
idiopathic pulmonary fibrosis
lung fibrosis
bleomycin model
- Grants
- 1 known grant, last ended Aug 2026
What they work on
- Test whether reducing lung stretch by paralyzing one side of the diaphragm slows fibrosis progression in the outer and lower lung of mice with bleomycin-induced lung injury.
- Compare how mechanical stretch affects bleomycin-induced fibrosis in young versus old mice, given that lung levels of Thy-1, a protein that senses mechanical force, decline with age.
- Identify the molecular and cellular mechanisms, including Thy-1 and integrin signaling, and candidate genes in specific lung cell types that connect breathing-related stretch to abnormal tissue remodeling.
More about the research
The center and upper regions are mostly spared, even though the team's earlier study of IPF lungs found disease-related gene activity there too. Why does scarring keep worsening only in some regions? One clue is that, even in healthy people, the outer and lower lung stretches much more with each breath than the central and upper lung.
Why it matters
IPF is a progressive disease that steadily reduces patients' quality of life. Explaining how breathing-related stretch drives scarring could identify cell-specific genes, possibly including the mechanical sensor Thy-1, as targets for preventing fibrosis progression and flare-ups. The new mouse model could also serve as a preclinical platform for testing therapies that act on mechanical signaling.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Margaret Thomas Freeberg
Virginia Commonwealth University, VA·Physiology·Early-career
Characterize how the mechanoreceptor Piezo2, a membrane channel that opens under mechanical force, drives metabolic adaptation to increased matrix stiffness, using lung fibroblasts from IPF and non-fibrotic donors.
Beiyun Zhou
University of Southern California, CA·Physiology
Identify how loss of the endoplasmic reticulum chaperone GRP78 disturbs mitochondrial energy production and biosynthesis in alveolar epithelial cells, and how this promotes pulmonary fibrosis, using AT2 cell-specific Grp78 knockout mice.
Yvonne M. W. Janssen-Heininger
University of Vermont, VT·Biochemistry
Determine whether the enzyme GSTP drives glutathionylation of OTUB1 and keeps KRT8-high transitional lung cells from maturing into AT1 cells, using a clinically tested GSTP inhibitor and IPF patient organoids.
The school
University of Virginia: 43 labs on PI Pages, $814M a year on research, 413 research doctorates a year.
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