ArticleeLife2023
Reciprocal interactions between alveolar progenitor dysfunction and aging promote lung fibrosis.
Article in eLife, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
26 citing papers in PubMed, 33 citations in OpenAlex.
- Syndecan-1 Promotes Alveolar Type 2 Epithelial Cell Senescence during Lung Fibrosis.bioRxiv : the preprint server for biology · 2026Article
- Lung mTOR activation leads to lung fibrosis or emphysema via senescence of specific lung cells.Scientific reports · 2026Article
- Cellular heterogeneity of HTII-280-labeled epithelial cells in healthy and fibrotic human lungs.American journal of respiratory and critical care medicine · 2026Article
- Conditional BCL-2 Expression in Fibroblasts Promotes Persistent Pulmonary Fibrosis which is Reversible by Therapeutic BCL-2 Inhibition.Nature communications · 2026Article
- Cellular plasticity and regenerative mechanisms in the lung.European respiratory review : an official journal of the European Respiratory Society · 2026Review
- Lipid metabolism as a cell-state determinant in pulmonary fibrosis: from epithelial failure to ferroptosis-driven amplification.Frontiers in pharmacology · 2026Review
- How stem cells respond to infection, inflammation and ageing.Nature reviews. Immunology · 2025Review
- Local photocrosslinking of native tissue matrix regulates lung epithelial cell mechanosensing and function.Nature materials · 2025Article
- Aging affects reprogramming of pulmonary capillary endothelial cells after lung injury in male mice.Nature communications · 2025Article
- The Hypoxia-Retinoid Axis in Idiopathic Pulmonary Fibrosis: Multifaceted Etiology and Therapeutic Potential.International journal of molecular sciences · 2025Review
- Article
- Development of delayed pulmonary toxicities and transcriptional changes in pre-existing interstitial lung disease mice after partial thoracic irradiation.Radiation oncology (London, England) · 2025Article
- Mitochondrial dysfunction and alveolar type II epithelial cell senescence: The destroyer and rescuer of idiopathic pulmonary fibrosis.Frontiers in cell and developmental biology · 2025Review
- Imperfect wound healing sets the stage for chronic diseases.Science (New York, N.Y.) · 2024Review
- Bi-directional regulation between inflammation and stem cells in the respiratory tract.Journal of cell science · 2024Review
- Article
- Aging-Associated Molecular Changes in Human Alveolar Type I Cells.Journal of respiratory biology and translational medicine · 2024Article
- Local photo-crosslinking of native tissue matrix regulates cell function.bioRxiv : the preprint server for biology · 2024Article
- Transcriptomics Analysis Identifies the Decline in the Alveolar Type II Stem Cell Niche in Aged Human Lungs.American journal of respiratory cell and molecular biology · 2024Article
- Lipid Deficiency Contributes to Impaired Alveolar Progenitor Cell Function in Aging and Idiopathic Pulmonary Fibrosis.American journal of respiratory cell and molecular biology · 2024Article
Corrections and comments
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Authors and funding
15 authors at 1 institution in 1 country.
Funding
Abstract
Aging is a critical risk factor in idiopathic pulmonary fibrosis (IPF). Dysfunction and loss of type 2 alveolar epithelial cells (AEC2s) with failed regeneration is a seminal causal event in the pathogenesis of IPF, although the precise mechanisms for their regenerative failure and demise remain unclear. To systematically examine the genomic program changes of AEC2s in aging and after lung injury, we performed unbiased single-cell RNA-seq analyses of lung epithelial cells from uninjured or bleomycin-injured young and old mice, as well as from lungs of IPF patients and healthy donors. We identified three AEC2 subsets based on their gene signatures. Subset AEC2-1 mainly exist in uninjured lungs, while subsets AEC2-2 and AEC2-3 emerged in injured lungs and increased with aging. Functionally, AEC2 subsets are correlated with progenitor cell renewal. Aging enhanced the expression of the genes related to inflammation, stress responses, senescence, and apoptosis. Interestingly, lung injury increased aging-related gene expression in AEC2s even in young mice. The synergistic effects of aging and injury contributed to impaired AEC2 recovery in aged mouse lungs after injury. In addition, we also identified three subsets of AEC2s from human lungs that formed three similar subsets to mouse AEC2s. IPF AEC2s showed a similar genomic signature to AEC2 subsets from bleomycin-injured old mouse lungs. Taken together, we identified synergistic effects of aging and AEC2 injury in transcriptomic and functional analyses that promoted fibrosis. This study provides new insights into the interactions between aging and lung injury with interesting overlap with diseased IPF AEC2 cells.
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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.