Beiyun Zhou
University of Southern California, CA·Physiology
Idiopathic pulmonary fibrosis (IPF) is a disease of aging in which scar tissue slowly replaces healthy lung, making breathing progressively harder; treatments remain limited. A leading idea is that the problem starts in the thin epithelial cells lining the lung's air sacs, which become damaged and stop maintaining the tissue.
- Fields
Physiology
Medicine & Clinical Research
Biochemistry
- Topics
idiopathic pulmonary fibrosis
endoplasmic reticulum stress
unfolded protein response
- Grants
- 1 known grant, through Dec 2026
What they work on
- 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.
- Characterize how reduced GRP78 drives an aging phenotype in alveolar epithelial cells — senescence, apoptosis, and abnormal mTOR signaling — and link it to fibrosis in mouse lungs and IPF patient cells.
- Test whether reactive oxygen species-induced carbonylation of GRP78, an oxidative protein modification seen in AT2 cells from IPF patients and aged mice, contributes to unresolved endoplasmic reticulum stress.
- Determine the therapeutic potential of targeting GRP78 loss-mediated metabolic and unfolded protein response pathways in age-associated pulmonary fibrosis, in mouse models and in cultured alveolar epithelial cells.
More about the research
This project asks why those cells fail with age, focusing on GRP78, a chaperone protein in the endoplasmic reticulum (the cell compartment where proteins are folded) that acts as a master regulator of protein quality control.
Why it matters
Patients with idiopathic pulmonary fibrosis face high mortality and few effective therapies. By tracing lung scarring back to loss of a single protein-folding chaperone and the metabolic and mTOR changes that follow, this work could identify drug targets that act selectively on the damaged, scar-promoting lung epithelial cells, providing a rationale for metabolism-directed treatments for this age-associated disease.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
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.
Timothy Blackwell
University of Michigan, MI·Medicine & Clinical Research
Detect gene activity biomarkers of pre-clinical disease in asymptomatic relatives of familial pulmonary fibrosis patients, using single-cell RNA sequencing of blood immune cells such as CD14+ monocytes alongside high-resolution CT findings.
Seunghye Han
Northwestern University, IL·Medicine & Clinical Research
Test whether a raised mitochondrial NADH/NAD+ ratio and the protein DELE1 are needed to activate the integrated stress response that blocks AT2-to-AT1 lung cell maturation when mitochondrial complex I is lost.
The school
University of Southern California: 47 labs on PI Pages, $1.3B a year on research, 882 research doctorates a year.
Reach out
A start for your email. Fill in the brackets.