ArticlePloS one2017
Myofibroblasts are increased in the lung parenchyma in asthma.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 44 citations in OpenAlex.
- PDGFRα+ fibroblast ablation exacerbates pathologic features in a model of house dust mite-induced allergenic asthma.Disease models & mechanisms · 2025Article
- YAP as a potential therapeutic target for myofibroblast formation in asthma.Respiratory research · 2025Article
- Review
- Interactions between epithelial mesenchymal plasticity, barrier dysfunction and innate immune pathways shape the genesis of allergic airway disease.Expert review of respiratory medicine · 2025Review
- Rhinovirus induces airway remodeling: what are the physiological consequences?Respiratory research · 2023Review
- Epithelial-Mesenchymal Transition Mechanisms in Chronic Airway Diseases: A Common Process to Target?International journal of molecular sciences · 2023Review
- PPARδ Agonist GW501516 Suppresses the TGF-β-Induced Profibrotic Response of Human Bronchial Fibroblasts from Asthmatic Patients.International journal of molecular sciences · 2023Article
- Pericytes: The lung-forgotten cell type.Frontiers in physiology · 2023Review
- Innate Immunity, Epithelial Plasticity, and Remodeling in Asthma.Advances in experimental medicine and biology · 2023Article
- Airway remodeling heterogeneity in asthma and its relationship to disease outcomes.Frontiers in physiology · 2023Review
- Cellular sources of airway smooth muscle cells in asthmatic airway remodeling and their clinical relevance: a narrative review.Annals of translational medicine · 2022Article
- Single-Cell RNA Sequencing Reveals the Interaction of Injected ADSCs with Lung-Originated Cells in Mouse Pulmonary Fibrosis.Stem cells international · 2022Article
- Review
- The Emerging Roles of π Subunit-Containing GABAInternational journal of medical sciences · 2021Review
- TWIST1 DNA methylation is a cell marker of airway and parenchymal lung fibroblasts that are differentially methylated in asthma.Clinical epigenetics · 2020Article
- IL-17 Induced Autophagy Regulates Mitochondrial Dysfunction and Fibrosis in Severe Asthmatic Bronchial Fibroblasts.Frontiers in immunology · 2020Article
- Transcriptomic changes during TGF-β-mediated differentiation of airway fibroblasts to myofibroblasts.Scientific reports · 2019Article
- Mechanisms how mucosal innate immunity affects progression of allergic airway disease.Expert review of respiratory medicine · 2019Review
- Mucosal bromodomain-containing protein 4 mediates aeroallergen-induced inflammation and remodeling.The Journal of allergy and clinical immunology · 2019Observational
- Efficacy of Novel Highly Specific Bromodomain-Containing Protein 4 Inhibitors in Innate Inflammation-Driven Airway Remodeling.American journal of respiratory cell and molecular biology · 2019Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIncreased airway smooth muscle is observed in large and small airways in asthma. Semi-quantitative estimates suggest that cells containing alpha smooth muscle actin (α-SMA) are also increased in the lung parenchyma. This study quantified and characterized α-SMA positive cells (α-SMA+) in the lung parenchyma of non-asthmatic and asthmatic individuals.
methodsPost-mortem sections of peripheral lung from cases of fatal asthma (FA), persons with asthma dying of non-respiratory causes (NFA) and non-asthma control subjects (NAC) were stained for α-SMA, quantified using point-counting and normalised to alveolar basement membrane length and interstitial area.
resultsα-SMA+ fractional area was increased in alveolar parenchyma in both FA (14.7 ± 2.8% of tissue area) and NFA (13.0 ± 1.2%), compared with NAC (7.4 ± 2.4%), p < 0.05 The difference was greater in upper lobes compared with lower lobes (p < 0.01) in both asthma groups. Similar changes were observed in alveolar ducts and alveolar walls. The electron microscopic features of the α-SMA+ cells were characteristic of myofibroblasts.
conclusionsWe conclude that in asthma there is a marked increase in α-SMA+ myofibroblasts in the lung parenchyma. The physiologic consequences of this increase are unknown.
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Registered trials
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