Seunghye Han, MD, MPH

Lung fibrosis is a devastating disorder that limits the lungs’ ability to extract oxygen due to progressive scarring. Affected patients eventually die from poor oxygen supply to the body. The few available therapies only slow disease progression without curing the disease. Mitochondria, small organelles responsible for energy generation and cellular signaling, do not function properly in patients with lung fibrosis. We have identified certain aspects of mitochondrial function that regulate the transformation of specific lung cells into oxygen-extracting cells. In a mouse model, we found that without proper mitochondrial functioning, the mice developed lung fibrosis. Their fibrosis was improved by a molecule targeting mitochondrial dysfunction. We will study in detail how lung cells behave with and without proper mitochondrial functioning by obtaining large-scale data on DNA expression and metabolite levels in mice. We will test this molecule in different animal models with a goal of validating mitochondrial function as a target for therapy to treat lung fibrosis.