ArticleRespiratory research2022
Impaired AT2 to AT1 cell transition in PM2.5-induced mouse model of chronic obstructive pulmonary disease.
Article in Respiratory research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.
What it found
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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
34 citing papers in PubMed, 1 synthesis or guideline pooled it, 60 citations in OpenAlex.
- The Efficacy and Safety of Budesonide/Glycopyrronium/Formoterol in the Treatment of COPD in the Elderly.Contrast media & molecular imaging · 2022Pooled it
- Heliox ventilation promotes pulmonary circulation and cardiac function in elderly hypertensive patients: a randomized controlled trial.Medical gas research · 2026Trial
- Engineered exosomes encapsulated miR-218-5p alleviate the progression of PMRedox biology · 2026Article
- Fuelling repair: metabolic regulation of alveolar type 2 cell fate in lung regeneration and disease.Disease models & mechanisms · 2026Review
- Targeting Elastin-Derived Peptides Reverses Alveolar Epithelial Dysfunction in Chronic Obstructive Pulmonary Disease.MedComm · 2026Article
- SERPINE1 drives ferroptosis in acute respiratory distress syndrome by disrupting mitochondrial NADRedox biology · 2026Article
- The triple-hit hypothesis: exploring pulmonary e-cigarette, PMEuropean respiratory review : an official journal of the European Respiratory Society · 2026Review
- Occupational Exposure to Factory-Derived Particulate Matter 2.5 Induces Cutaneous Toxicity in Workers and HaCaT Keratinocytes Through Oxidative Stress and Inflammation.Journal of applied toxicology : JAT · 2026Article
- Epithelial cells in chronic obstructive pulmonary disease exacerbations: Targets for lung repair.Pharmacological reviews · 2026Review
- Regenerative therapeutics for chronic obstructive pulmonary disease.Pharmacological reviews · 2026Review
- Single-Cell RNA Sequencing of Human Lung Tissues Reveals Metallothionein-Positive T Cells as a Novel Potential Marker of Susceptibility to Chronic Obstructive Pulmonary Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Article
- Epidemiological Trends and Projections of PMInternational journal of chronic obstructive pulmonary disease · 2026Article
- Lung scRNA-seq reveals chronic inflammation and emphysemous phenotype in mice with osteogenesis imperfecta.Frontiers in genetics · 2026Article
- USP18 confers protection against allergic asthma by suppressing CCL8 production in alveolar type II epithelial cells.Respiratory research · 2025Article
- Recent Applications of Lung Organoid and Lung-on-a-Chip Technologies for Evaluating the Toxicity of Fine Particulate Matter.International journal of stem cells · 2025Review
- Article
- Impact of long-term exposure to PMBMC public health · 2025Article
- Nrf2 pathway potentially confers protection against cigarette smoke-induced sarcopenia in a mouse model.European journal of medical research · 2025Article
- Building blocks for lung regeneration: Stem cells and niches.Molecules and cells · 2025Review
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundParticular matter 2.5 (PM2.5) is one of the most important air pollutant, and it is positively associated with the development of chronic obstructive pulmonary disease (COPD). However, the precise underlying mechanisms through which PM2.5 promotes the development of COPD remains largely unknown.
methodsMouse alveolar destruction were determined by histological analysis of lung tissues and lung function test. Alveolar type II cells (AT2) to alveolar type I cells (AT1) transition in PM2.5-induced COPD mouse model was confirmed via immunofluorescence staining and qPCR analysis. The differentially expressed genes in PM2.5-induced COPD mouse model were identified by RNA-sequencing of alveolar epithelial organoids and generated by bioinformatics analysis.
resultsIn this study, we found that 6 months exposure of PM2.5 induced a significantly decreased pulmonary compliance and resulted in pulmonary emphysema in mice. We showed that PM2.5 exposure significantly reduced the AT2 to AT1 cell transition in vitro and in vivo. In addition, we found a reduced expression of the intermediate AT2-AT1 cell process marker claudin 4 (CLDN4) at day 4 of differentiation in mouse alveolar organoids treated with PM2.5, suggesting that PM2.5 exposure inhibited AT2 cells from entering the transdifferentiation process. RNA-sequencing of mouse alveolar organoids showed that several key signaling pathways that involved in the AT2 to AT1 cell transition were significantly altered including the Wnt signaling, MAPK signaling and signaling pathways regulating pluripotency of stem cells following PM2.5 exposure.
conclusionsIn summary, these data demonstrate a critical role of AT2 to AT1 cell transition in PM2.5-induced COPD mouse model and reveal the signaling pathways that potentially regulate AT2 to AT1 cell transition during this process. Our findings therefore advance the current knowledge of PM2.5-induced COPD and may lead to a novel therapeutic strategy to treat this disease.
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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.