The failure of lung epithelial cells to complete transition from a stem cell-like state into a fully differentiated state causes lung fibrosis, according to a Northwestern Medicine study published in Proceedings of the National Academy of the Sciences (PNAS).
Administering a small molecule to mice with lung fibrosis helped complete this cellular transition in both young and old mice, suggesting it could become part of therapy in the future, according to Alexander Misharin, MD, PhD, assistant professor of Medicine in the Division of Pulmonary and Critical Care and co-senior author of the study.
“Currently, therapeutic options for patients with pulmonary fibrosis are limited to lung transplantation and two drugs with modest efficacy and severe side effects, so new drugs that could slow down progression or revert pulmonary fibrosis are much needed,” Misharin said.
Pulmonary fibrosis is a condition in which lung tissue becomes damaged and scarred, gradually and irreversibly eroding lung function. Misharin and his collaborators examined cells in the lung epithelium, including flat type 1 epithelial cells, which are involved in gas exchange between the lung alveoli and the blood, and cuboidal type 2 cells, which normally produce surfactant.
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Proceedings of the National Academy of the Sciences. Study Paper: