ArticleAmerican journal of physiology. Lung cellular and molecular physiology2013
Differential susceptibility of inbred mouse strains to chlorine-induced airway fibrosis.
Article in American journal of physiology. Lung cellular and molecular physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.
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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
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
30 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.
- Phosgene-Induced acute lung injury: Approaches for mechanism-based treatment strategies.Frontiers in immunology · 2022Pooled it
- Characteristics of phosgene aspiration lung injury analyzed based on transcriptomics and proteomics.Frontiers in genetics · 2024Article
- Pulmonary endogenous progenitor stem cell subpopulation: Physiology, pathogenesis, and progress.Journal of intensive medicine · 2023Review
- Halogen-Induced Chemical Injury to the Mammalian Cardiopulmonary Systems.Physiology (Bethesda, Md.) · 2021Review
- Toxic effects of chlorine gas and potential treatments: a literature review.Toxicology mechanisms and methods · 2021Review
- Effects of metal nanoparticles on tight junction-associated proteins via HIF-1α/miR-29b/MMPs pathway in human epidermal keratinocytes.Particle and fibre toxicology · 2021Article
- miR-21 mediates nickel nanoparticle-induced pulmonary injury and fibrosis.Nanotoxicology · 2020Article
- Halogen exposure injury in the developing lung.Annals of the New York Academy of Sciences · 2020Review
- Hyaluronan and halogen-induced airway hyperresponsiveness and lung injury.Annals of the New York Academy of Sciences · 2020Review
- Phosgene inhalation causes hemolysis and acute lung injury.Toxicology letters · 2019Article
- Inhibition of chlorine-induced airway fibrosis by budesonide.Toxicology and applied pharmacology · 2019Article
- Comparative mouse lung injury by nickel nanoparticles with differential surface modification.Journal of nanobiotechnology · 2019Article
- Halogen Inhalation-Induced Lung Injury and Acute Respiratory Distress Syndrome.Chinese medical journal · 2018Review
- An Official American Thoracic Society Workshop Report: Chemical Inhalational Disasters. Biology of Lung Injury, Development of Novel Therapeutics, and Medical Preparedness.Annals of the American Thoracic Society · 2017Article
- Acute lung injury and persistent small airway disease in a rabbit model of chlorine inhalation.Toxicology and applied pharmacology · 2017Article
- Sex difference in EGFR pathways in mouse kidney-potential impact on the immune system.BMC genetics · 2016Article
- Proteomic identification of cyclophilin A as a potential biomarker and therapeutic target in oral submucous fibrosis.Oncotarget · 2016Article
- Persistent effects of chlorine inhalation on respiratory health.Annals of the New York Academy of Sciences · 2016Review
- Heme Attenuation Ameliorates Irritant Gas Inhalation-Induced Acute Lung Injury.Antioxidants & redox signaling · 2016Article
- Sex Difference of Egfr Expression and Molecular Pathway in the Liver: Impact on Drug Design and Cancer Treatments?Journal of Cancer · 2016Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Chlorine is a reactive gas that is considered a chemical threat agent. Humans who develop acute lung injury from chlorine inhalation typically recover normal lung function; however, a subset can experience chronic airway disease. To examine pathological changes following chlorine-induced lung injury, mice were exposed to a single high dose of chlorine, and repair of the lung was analyzed at multiple times after exposure. In FVB/NJ mice, chlorine inhalation caused pronounced fibrosis of larger airways that developed by day 7 after exposure and was associated with airway hyperreactivity. In contrast, A/J mice had little or no airway fibrosis and had normal lung function at day 7. Unexposed FVB/NJ mice had less keratin 5 staining (basal cell marker) than A/J mice in large intrapulmonary airways where epithelial repair was poor and fibrosis developed after chlorine exposure. FVB/NJ mice had large areas devoid of epithelium on day 1 after exposure leading to fibroproliferative lesions on days 4 and 7. A/J mice had airways covered by squamous keratin 5-stained cells on day 1 that transitioned to a highly proliferative reparative epithelium by day 4 followed by the reappearance of ciliated and Clara cells by day 7. The data suggest that lack of basal cells in the large intrapulmonary airways and failure to effect epithelial repair at these sites are factors contributing to the development of airway fibrosis in FVB/NJ mice. The observed differences in susceptibility to chlorine-induced airway disease provide a model in which mechanisms and treatment of airway fibrosis can be investigated.
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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.