ArticleJCI insight2025
Regulation of lung progenitor plasticity and repair by fatty acid oxidation.
Article in JCI insight, 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.
- Integration of clinical variables and CT radiomics features in a nomogram for predicting interstitial lung disease in Sjögren's syndrome.Journal of thoracic disease · 2026Article
- The landscape of protein post-translational modifications in the pathogenesis of acute respiratory distress syndrome.Journal of thoracic disease · 2026Review
- The Gut-Lung Microbiome Axis in Alveolar Stem Cell Regeneration and Lung Repair.Microorganisms · 2026Review
- Alveolar Epithelial Cell Loss of the Mitochondrial Regulator TFAM Drives Progressive Lung Fibrosis.bioRxiv : the preprint server for biology · 2026Article
- Fueling the fire: metabolic dysfunction and senescence as drivers of lung aging and disease.Physiological reviews · 2026Review
- Unraveling the layers of epigenetic control in respiratory antiviral defense.Journal of virology · 2026Review
- Enhanced fatty acid availability rewires fibroblasts metabolism and decreases collagen deposition in lung fibrosis.Cellular and molecular life sciences : CMLS · 2026Article
- Hallmarks of the ageing lung: 10 years later.The European respiratory journal · 2026Review
- Review
- ACSBG1‑driven lipid reprogramming unveiled: A fatty acid metabolism‑associated prognostic model for lung adenocarcinoma.Oncology reports · 2026Article
- Alveolar type 2 cell LRP1 is needed for surfactant phospholipid metabolism and pulmonary function in mice.Journal of lipid research · 2026Article
- Unraveling the temporal dynamics of radiation-induced lung injury: a multi-omics integration of transcriptomic, proteomic, and metabolic reprogramming.BMC medical genomics · 2026Article
- The Sixth Annual Symposium of the Midwest Aging Consortium.The journals of gerontology. Series A, Biological sciences and medical sciences · 2026Article
- Pulmonary Vascular Endothelial Cells in Lung Diseases: Mechanisms, Therapeutic Strategies, and Future Directions.Cell proliferation · 2026Review
- Lipid metabolism as a cell-state determinant in pulmonary fibrosis: from epithelial failure to ferroptosis-driven amplification.Frontiers in pharmacology · 2026Review
- Lipid droplet-mitochondria contact sites as druggable spatial-pharmacology targets in respiratory disease: cross-cell-type mechanisms and translational strategies.Frontiers in cell and developmental biology · 2026Review
- Generation of alveolar organoids from human induced pluripotent stem cells using a stirred-tank bioreactor.Frontiers in bioengineering and biotechnology · 2026Article
- Serum metabolic characteristics of interstitial lung disease: a potential link between endocrine aging and gut-derived metabolites.Frontiers in medicine · 2026Article
- Impaired AMPK control of alveolar epithelial cell metabolism promotes pulmonary fibrosis.JCI insight · 2025Article
- Mechanisms and markers of lung ageing in health and disease.European respiratory review : an official journal of the European Respiratory Society · 2025Review
Corrections and comments
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Authors and funding
22 authors.
Funding
Abstract
Idiopathic pulmonary fibrosis (IPF) is an age-related interstitial lung disease, characterized by inadequate alveolar regeneration and ectopic bronchiolization. While some molecular pathways regulating lung progenitor cells have been described, the role of metabolic pathways in alveolar regeneration is poorly understood. We report that expression of fatty acid oxidation (FAO) genes is significantly diminished in alveolar epithelial cells of IPF lungs by single-cell RNA sequencing and tissue staining. Genetic and pharmacological inhibition in AT2 cells of carnitine palmitoyltransferase 1a (CPT1a), the rate-limiting enzyme of FAO, promoted mitochondrial dysfunction and acquisition of aberrant intermediate states expressing basaloid, and airway secretory cell markers SCGB1A1 and SCGB3A2. Furthermore, mice with deficiency of CPT1a in AT2 cells show enhanced susceptibility to developing lung fibrosis with an accumulation of epithelial cells expressing markers of intermediate cells, airway secretory cells, and senescence. We found that deficiency of CPT1a causes a decrease in SMAD7 protein levels and TGF-β signaling pathway activation. These findings suggest that the mitochondrial FAO metabolic pathway contributes to the regulation of lung progenitor cell repair responses and deficiency of FAO contributes to aberrant lung repair and the development of lung fibrosis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.