ArticleCell death & disease2019
Airway epithelial regeneration requires autophagy and glucose metabolism.
Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
47 citing papers in PubMed, 78 citations in OpenAlex.
- ZKSCAN3 mitigates lipopolysaccharide-induced acute lung injury by restraining excessive autophagy via activation of the mTOR pathway.Journal of thoracic disease · 2026Article
- Breaking the bottleneck of asthma treatment: the future of omni-targeted therapy.Journal of advanced research · 2026Review
- Research Advances and Disease Modeling in Respiratory Organoids.Biomedicines · 2026Review
- Mitochondrial pyruvate metabolism in club cells drives airway inflammation.Stem cell reports · 2026Article
- Quantitative proteomics links mitochondrial dysfunction to metabolic changes and epithelial differentiation defects in hyperoxia-exposed neonatal airway cells.American journal of physiology. Lung cellular and molecular physiology · 2026Article
- Article
- Autophagy in Acute Lung Injury.Cell biochemistry and biophysics · 2025Review
- Diabetes mellitus-driven pulmonary injury: multidimensional mechanisms linking metabolic dysregulation to gut-lung axis and promising therapies.Frontiers in pharmacology · 2025Review
- Autophagy in the lung: guardian of homeostasis or driver of disease.Autophagy reports · 2025Review
- Research Progress on Glycolysis in the Pathogenesis of Asthma.Journal of asthma and allergy · 2025Review
- Targeting alveolar epithelial cell metabolism in pulmonary fibrosis: Pioneering an emerging therapeutic strategy.Frontiers in cell and developmental biology · 2025Review
- Unlocking lung regeneration: insights into progenitor cell dynamics and metabolic control.Cell regeneration (London, England) · 2024Review
- A narrative review on lung injury: mechanisms, biomarkers, and monitoring.Critical care (London, England) · 2024Review
- ECM and epithelial stem cells: the scaffold of destiny.Frontiers in cell and developmental biology · 2024Review
- Progress and Gaps in Respiratory Disease Research and Treatment: Highlights of the IRM 2024 in Shanghai.Journal of respiratory biology and translational medicine · 2024Article
- Nitric oxide hinders club cell proliferation through Gdpd2 during allergic airway inflammation.FEBS open bio · 2023Article
- Repair of airway epithelia requires metabolic rewiring towards fatty acid oxidation.Nature communications · 2023Article
- Pulmonary endogenous progenitor stem cell subpopulation: Physiology, pathogenesis, and progress.Journal of intensive medicine · 2023Review
- Pathogenesis and treatment of chronic rhinosinusitis from the perspective of sinonasal epithelial dysfunction.Frontiers in medicine · 2023Review
- New insights into autophagy in inflammatory subtypes of asthma.Frontiers in immunology · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Efficient repair of injured epithelium by airway progenitor cells could prevent acute inflammation from progressing into chronic phase in lung. Here, we used small molecules, genetic loss-of-function, organoid cultures, and in vivo lung-injury models to show that autophagy is essential for maintaining the pool of airway stem-like vClub cells by promoting their proliferation during ovalbumin-induced acute inflammation. Mechanistically, impaired autophagy disrupted glucose uptake in vClub progenitor cells, and either reduced accessibility to glucose or partial inhibition of glycolysis promoted the proliferative capacity of vClub progenitor cells and their daughter Club cells. However, glucose deprivation or glycolysis blockade abrogated the proliferative capacity of airway vClub cells and Club cells but promoted ciliated and goblet cell differentiation. Deficiency of glucose transporter-1 suppressed the proliferative capacity of airway progenitor cells after ovalbumin challenge. These findings suggested that autophagy and glucose metabolism are essential for the maintenance of airway epithelium at steady state and during allergic inflammation.
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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.