ArticlebioRxiv : the preprint server for biology2026
Chronic TGFβ1 Signaling Drives Aberrant Alveolar-Basaloid Metaplasia through a KRT17-Stratifin migratory complex.
Article in bioRxiv : the preprint server for biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Authors and funding
14 authors.
Funding
Abstract
Chronic fibrotic disorders like idiopathic pulmonary fibrosis (IPF) are characterized by aberrant alveolar regeneration and severely limited treatment options. Identification of the mechanisms driving aberrant epithelial repair can lead to new viable therapeutic targets. Using integrated single nucleus ATAC- and RNA-sequencing on human lungs and an in vitro model of dysplastic repair, we identify two distinct regenerative trajectories for alveolar type 2 (AT2) cells: a resolvable euplastic repair trajectory and a persistent, non-resolving dysplastic repair trajectory. The latter is governed by a spatially restricted ITGB6/TGFβ1/SMAD3 signaling axis in fibrotic regions of IPF lungs and in murine lungs characterized by chronic epithelial remodeling. Mechanistically, SMAD3 directly regulates dysplastic transitional cell (DTC) markers, including KRT17 and Stratifin. We show that TGFβ1 signaling promotes a physical interaction between KRT17 and Stratifin at the leading edge of migrating DTCs
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