NIH R01 · 2024
Targeting dysfunctional epithelial repair in pulmonary fibrosis
While it is generally agreed that epithelial injury is a central process in Idiopathic Pulmonary Fibrosis (IPF), differential mechanisms that determine functional repair versus dysfunctional repair are incompletely understood. Emerging data indicate that airway-derived progenitors can give rise to a variety of “transitional” and proximal-like cell states that are retained in the lung parenchyma in humans with IPF, thereby suggesting that these aberrant epithelial cell states contribute to dysfunctional repair following repetitive injury. This proposal is focused on elucidating the mediators and pathways that contribute to dysfunctional epithelial phenotypes that emerge in persistent lung…
From the public funding record at NIH RePORTER. Describes the funded project, not the reviews below.