STL1267 inhibits myofibroblast differentiation in a TGFβ1-driven human lung fibroblast model
Abstract
This study introduces a novel in vitro adenovirus-based model of persistent TGFβ1 signaling in normal human lung fibroblasts to mimic chronic fibrosis. Using this model, we show that the next-generation REV-ERBα agonist STL1267 robustly inhibits myofibroblast differentiation and ECM gene expression. STL1267 outperforms Food and Drug Administration-approved antifibrotic drugs and modulates immune and circadian signaling pathways, supporting its potential as a promising circadian-based therapeutic strategy for pulmonary fibrosis.
Fields of Study & Subjects
Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
Neonatal Respiratory Health Research
Lung Cancer Treatments and Mutations
Publication details
- Journal / source
- American Journal of Physiology-Cell Physiology
- Volume
- 330
- Issue
- 3
- Pages
- C571–C589
- Publication date
- 9 January 2026
- Language
- EN