ArticleScience translational medicine2025
Hypoxia-inducible factor 2 regulates alveolar regeneration after repetitive injury in three-dimensional cellular and in vivo models.
Article in Science translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed.
- Sustained YAP/TAZ activation promotes aberrant alveolar epithelial cell differentiation and drives persistent fibrotic remodeling.JCI insight · 2026Article
- From data mining to mechanistic prediction: a study on drug-induced lung injury integrating FAERS, machine learning, and network toxicology.Archives of toxicology · 2026Article
- UBE2M deficiency in alveolar macrophages promotes emphysema through HIF-2α/MMP12 axis.Chinese medical journal pulmonary and critical care medicine · 2026Article
- Hallmarks of the ageing lung: 10 years later.The European respiratory journal · 2026Review
- Reparative "exosome-ark" for mitochondrial transplantation to reprogram macrophages and disrupt pathogenic crosstalk in pulmonary fibrosis.Materials today. Bio · 2026Article
- 2025 annual review of basic and translational research advances in pulmonary fibrosis: a narrative review.Journal of thoracic disease · 2026Review
- Chronic TGFβ1 Signaling Drives Aberrant Alveolar-Basaloid Metaplasia through a KRT17-Stratifin migratory complex.bioRxiv : the preprint server for biology · 2026Article
- The chromatin remodeling complex PRC2 safeguards cell fate in alveolar epithelial type 2 cells.bioRxiv : the preprint server for biology · 2026Article
- New approaches to uncover COPD pathobiology and develop therapies.JCI insight · 2026Review
- Convergent hub pathways targeted by IAV, SARS-CoV-2, and RSV in type II alveolar epithelial cells: molecular mechanisms and therapeutic implications.Frontiers in immunology · 2026Review
- Targeting the epithelium in pulmonary fibrosis.European respiratory review : an official journal of the European Respiratory Society · 2026Review
- Modulation of an aberrant basal cell program in human alveolar epithelial spheroids and lung slices.Respiratory research · 2025Article
- A ferret model demonstrates sustained fibrosis, restrictive physiology, and airway proximalization.NPJ Regenerative medicine · 2025Article
- Ferret model of bleomycin-induced lung injury shares features of human idiopathic pulmonary fibrosis.NPJ Regenerative medicine · 2025Article
- Hypoxia promotes airway differentiation in the human lung epithelium.Cell stem cell · 2025Article
- Pharmacologic inhibition of IRE1α-dependent decay protects alveolar epithelial identity and prevents pulmonary fibrosis in mice.The Journal of clinical investigation · 2025Article
- Paradigms, innovations, and biological applications of RNA velocity: a comprehensive review.Briefings in bioinformatics · 2025Review
- The Hypoxia-Retinoid Axis in Idiopathic Pulmonary Fibrosis: Multifaceted Etiology and Therapeutic Potential.International journal of molecular sciences · 2025Review
- A novel human fetal lung-derived alveolar organoid model reveals mechanisms of surfactant protein C maturation relevant to interstitial lung disease.The EMBO journal · 2025Article
- Biomarker-defined endotypes of pulmonary fibrosis.The Lancet. Respiratory medicine · 2024Article
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Authors and funding
16 authors.
Funding
Abstract
Idiopathic pulmonary fibrosis (IPF) is a progressive interstitial lung disease in which repetitive epithelial injury and incomplete alveolar repair result in accumulation of profibrotic intermediate/transitional "aberrant" epithelial cell states. The mechanisms leading to the emergence and persistence of aberrant epithelial populations in the distal lung remain incompletely understood. By interrogating single-cell RNA sequencing (scRNA-seq) data from patients with IPF and a mouse model of repeated lung epithelial injury, we identified persistent activation of hypoxia-inducible factor (HIF) signaling in these aberrant epithelial cells. Using mouse genetic lineage-tracing strategies together with scRNA-seq, we found that these disease-emergent aberrant epithelial cells predominantly arose from airway-derived (
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