Yutong Zhao
Ohio State University, OH·Medicine & Clinical Research
Lung diseases driven by runaway inflammation or runaway scarring remain hard to treat. Two projects examine the molecular controls inside lung cells that decide how these diseases progress.
- Fields
Medicine & Clinical Research
Biochemistry
Physiology
- Topics
acute respiratory distress syndrome
sepsis
acute lung injury
- Grants
- 2 known grants, through Nov 2028
What they work on
- Test whether blocking the mitochondrial deubiquitinase USP30 in endothelial cells reduces white blood cell adhesion and migration and preserves the vessel barrier, and whether deleting it lessens Pseudomonas- or sepsis-induced lung injury in mice.
- Determine how USP30 inhibition destabilizes the enzyme MAT2A, lowers SAM production and reduces methylation of the pri-miR-30 promoter, raising levels of the gene-silencing small RNA miR-30a-5p.
- Test whether miR-30a-5p explains the protection from USP30 loss, using human lung microvascular endothelial cells and RNA nanoparticles in mouse lung injury, and whether it lowers MDM2, MLC and NFAT5.
- Identify where the E3 ligase Nedd4L binds and ubiquitinates the BMP receptor BMPRII, and how K63-linked ubiquitin chains control BMPRII internalization and stability.
- Determine whether loss of Nedd4L is required for BMPRII breakdown triggered by TGF-β1 and lipid peroxidation, two drivers of lung fibrosis.
- Test whether Nedd4L promotes myofibroblast de-differentiation and fibrosis resolution by stabilizing BMPRII, using cultured lung myofibroblasts and fibroblast-specific inducible Nedd4L knockout mice.
More about the research
Both projects focus on ubiquitin, a small protein tag that marks other proteins for destruction or redirects them. One project studies enzymes that remove the tag (deubiquitinases). The other studies enzymes that add it (E3 ligases). The first project looks at blood vessel lining cells in acute lung injury. The second looks at scar-forming cells in pulmonary fibrosis.
Why it matters
ARDS and sepsis, often triggered by bacterial or viral infections, still have high death rates and no effective drugs. Idiopathic pulmonary fibrosis has no treatment that reverses scarring. These projects could identify new therapeutic targets: USP30 inhibition to protect blood vessel linings during acute lung inflammation, and the Nedd4L–BMPRII pathway to help scarred lungs heal, with possible benefit to patients with these lung diseases.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Jamie Meegan
University of South Alabama, AL·Physiology·Early-career
Test whether cell-free hemoglobin released from fragile red blood cells during sepsis disrupts the lung microvascular endothelial cell barrier by oxidizing low-density lipoprotein to oxidized LDL.
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.
Patrick Belvitch
University of Illinois Chicago, IL·Medicine & Clinical Research
Determine how CARMIL1, a regulator of actin filament growth, shapes edge actin structures in lung endothelial cells, using biochemistry and advanced imaging after silencing CARMIL1 or overexpressing normal or variant forms.
The school
Ohio State University: 71 labs on PI Pages, $1.6B a year on research, 882 research doctorates a year.
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