Seunghye Han
Northwestern University, IL·Medicine & Clinical Research
After severe pneumonia, such as COVID-19 pneumonia, some patients' lungs heal completely, while others develop lasting symptoms or progressive scarring (fibrosis) that can be fatal or require a lung transplant. Why patients with similar injuries end up so differently is unknown.
- Fields
Medicine & Clinical Research
Physiology
Biochemistry
- Topics
pulmonary fibrosis
lung fibrosis
acute respiratory distress syndrome
- Grants
- 1 known grant, through Aug 2029
What they work on
- 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.
- Determine whether activation of ATF4, a stress-response transcription factor, in lung epithelial cells is necessary and/or sufficient to impair AT2-to-AT1 differentiation, using genetic mouse models.
- Link mitochondrial metabolism and stress-response activation to lung fibrosis using NDUFS2-deficient mice and lung samples from pulmonary fibrosis patients at transplant.
More about the research
One clue is that mitochondria, the cell's energy and metabolism centers, malfunction in both severe pneumonia and lung fibrosis. Whether that malfunction actually causes failed lung repair has not been shown.
Why it matters
Patients who survive severe viral pneumonia or acute respiratory distress syndrome (ARDS) can develop progressive lung fibrosis, which may lead to death or lung transplantation. Showing that mitochondrial metabolism and the integrated stress response block lung repair could establish them as drug targets. That could lead to treatments that prevent or treat lung fibrosis.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Chitaru Kurihara
Northwestern University, IL·Medicine & Clinical Research
Determine whether integrated stress response activation of ATF4, a stress-induced gene regulator, is necessary for impaired alveolar epithelial repair after lung transplantation, using mouse transplant models.
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.
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.
The school
Northwestern University: 71 labs on PI Pages, $1.3B a year on research, 536 research doctorates a year.
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