ArticleAmerican journal of respiratory and critical care medicine2008
Lung fibroblast repair functions in patients with chronic obstructive pulmonary disease are altered by multiple mechanisms.
Article in American journal of respiratory and critical care medicine, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers.
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Who cites it
107 citing papers in PubMed, 201 citations in OpenAlex.
- Regenerative therapeutics for chronic obstructive pulmonary disease.Pharmacological reviews · 2026Review
- Increased total plasma TGF-β1 levels and deregulated IgA-IgM axis in chronic obstructive pulmonary disease.Journal of medical biochemistry · 2026Article
- Post-COPD: Can Emphysema Be Repaired?American journal of respiratory and critical care medicine · 2025Article
- Dissecting cross-population polygenic heterogeneity across respiratory and cardiometabolic diseases.Nature communications · 2025Article
- Fibroblast-derived osteoglycin promotes epithelial cell repair.NPJ Regenerative medicine · 2025Article
- Low Prostaglandin EJournal of clinical medicine · 2024Review
- MiR-1307-5p enhances fibroblast transdifferentiation to exacerbate chronic obstructive pulmonary disease through regulating FBXL16/HIF1α axis.Respiratory research · 2024Article
- The Role of the Extracellular Matrix in the Pathogenesis and Treatment of Pulmonary Emphysema.International journal of molecular sciences · 2024Review
- PTGES is involved in myofibroblast differentiation via HIF-1α-dependent glycolysis pathway.Journal of cellular and molecular medicine · 2024Article
- Emerging roles of senolytics/senomorphics in HIV-related co-morbidities.Biochemical pharmacology · 2024Review
- Human iPSC-Based Model of COPD to Investigate Disease Mechanisms, Predict SARS-COV-2 Outcome, and Test Preventive Immunotherapy.Stem cells (Dayton, Ohio) · 2024Article
- Small airway fibroblasts from patients with chronic obstructive pulmonary disease exhibit cellular senescence.American journal of physiology. Lung cellular and molecular physiology · 2024Article
- DNA nanoparticles targeting FOXO4 selectively eliminate cigarette smoke-induced senescent lung fibroblasts.Nanoscale advances · 2023Article
- Putative Bidirectionality of Chronic Obstructive Pulmonary Disease and Periodontal Disease: A Review of the Literature.Journal of clinical medicine · 2023Review
- Epithelial-Mesenchymal Transition Mechanisms in Chronic Airway Diseases: A Common Process to Target?International journal of molecular sciences · 2023Review
- Supersulphides provide airway protection in viral and chronic lung diseases.Nature communications · 2023Article
- High-resolution transcriptomic and epigenetic profiling identifies novel regulators of COPD.The EMBO journal · 2023Article
- Cystic fibrosis transmembrane conductance regulator in COPD: a role in respiratory epithelium and beyond.The European respiratory journal · 2023Review
- Circadian disruption in lung fibroblasts enhances NF-κB activity to exacerbate neutrophil recruitment.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023Article
- Extracellular Vesicle-Encapsulated microRNAs as Novel Biomarkers of Lung Health.American journal of respiratory and critical care medicine · 2023Article
47 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
16 authors at 4 institutions in 4 countries.
Funding
Abstract
rationaleFibroblasts are believed to be the major cells responsible for the production and maintenance of extracellular matrix. Alterations in fibroblast functional capacity, therefore, could play a role in the pathogenesis of pulmonary emphysema, which is characterized by inadequate maintenance of tissue structure.
objectivesTo evaluate the hypothesis that deficient fibroblast repair characterizes cells obtained from individuals with chronic obstructive pulmonary disease (COPD) compared with control subjects.
methodsFibroblasts were cultured from lung tissue obtained from individuals undergoing thoracotomy and were characterized in vitro. MEASUREMENTS AND MAIN
resultsFibroblasts from individuals with COPD, defined by reduced FEV(1), manifested reduced chemotaxis toward fibronectin and reduced contraction of three-dimensional collagen gels, two bioassays associated with fibroblast repair function. At least two mechanisms appear to account for these differences. Prostaglandin E (PGE), a known inhibitor of fibroblast repair functions, was produced in increased amount by fibroblasts from subjects with COPD, which also expressed increased amounts of the receptors EP2 and EP4, both of which signal through cyclic AMP. Incubation of fibroblasts with indomethacin or with the PKA inhibitor KT-5720 partially restored COPD subject fibroblast function. In addition, fibroblasts from subjects with COPD produced more transforming growth factor (TGF)-beta1, but manifested reduced response to TGF-beta1. The functional alterations in fibroblasts correlated with both lung function assessed by FEV(1) and, for the data available, with severity of emphysema assessed by Dl(CO).
conclusionsFibroblasts from individuals with COPD have reduced capability to sustain tissue repair, which suggests that this may be one mechanism that contributes to the development of emphysema.
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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.