IRE1α Drives Lung Epithelial Progenitor Dysfunction to Establish a Niche for Pulmonary Fibrosis

Kinase inhibitor of IRE1α treatment increased the differentiation of Krt19CreERT2-lineage-traced damage-associated transient progenitors (DATPs) into type 1 alveolar epithelial cells after bleomycin injury, indicating that relief from IRE1α signaling enabled DATPs to exit the transitional state.