ArticleLaboratory investigation; a journal of technical methods and pathology2018
Heparin-binding epidermal growth factor contributes to COPD disease severity by modulating airway fibrosis and pulmonary epithelial-mesenchymal transition.
Article in Laboratory investigation; a journal of technical methods and pathology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed, 32 citations in OpenAlex.
- The role of programmed cell death in chronic obstructive pulmonary disease: from pathogenesis to treatment.Frontiers in immunology · 2026Review
- CFTR I556V Variant Exacerbates Cigarette Smoke-Induced Airway Inflammation in COPD by Promoting NLRP3 Inflammasome Activation.International journal of chronic obstructive pulmonary disease · 2026Article
- A Novel In Vitro Potency Assay Demonstrating the Anti-Fibrotic Mechanism of Action of CDCs in Deramiocel.Biomedicines · 2025Article
- Fibroblast EGFR signaling mediates ricin toxin-induced acute lung injury via EGR1/CXCL1 axis.Archives of toxicology · 2025Article
- Airway remodeling in chronic obstructive pulmonary disease: characteristics and opportunities.Frontiers in medicine · 2025Review
- Smad7 ameliorate small airway remodeling in COPD by modulating epithelial-mesenchymal transition.Tobacco induced diseases · 2025Article
- Pathogenic Cell in COPD: Mechanisms of Airway Remodeling, Immune Dysregulation, and Therapeutic Implications.International journal of chronic obstructive pulmonary disease · 2025Review
- Protective Effect of the Total Alkaloid Extract from BulbusInternational journal of chronic obstructive pulmonary disease · 2024Article
- Keratin 15 protects against cigarette smoke-induced epithelial mesenchymal transformation by MMP-9.Respiratory research · 2023Article
- A blood and bronchoalveolar lavage protein signature of rapid FEVScientific reports · 2023Article
- Identification of the shared genes and immune signatures between systemic lupus erythematosus and idiopathic pulmonary fibrosis.Hereditas · 2023Article
- Article
- HB-EGF-induced IL-8 secretion from airway epithelium leads to lung fibroblast proliferation and migration.BMC pulmonary medicine · 2021Article
- Article
- Heparin-binding epidermal growth factor (HB-EGF) drives EMT in patients with COPD: implications for disease pathogenesis and novel therapies.Laboratory investigation; a journal of technical methods and pathology · 2019Review
- Epithelial-mesenchymal transition is driven by transcriptional and post transcriptional modulations in COPD: implications for disease progression and new therapeutics.International journal of chronic obstructive pulmonary disease · 2019Article
- Epithelial mesenchymal transition (EMT): a universal process in lung diseases with implications for cystic fibrosis pathophysiology.Respiratory research · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although airway fibrosis and epithelial-mesenchymal transition (EMT) contribute to airway remodeling in chronic obstructive pulmonary disease (COPD), the mechanisms underlying their development have not been fully elucidated. In the present study, we aimed to assess heparin-binding epidermal growth factor (HB-EGF) expression in the airways of patients with COPD and to elucidate the possible role of HB-EGF in the pathology of COPD. Sputum and lung tissue HB-EGF expression was evaluated in control subjects and patients with COPD. The relationships between HB-EGF expression, disease severity, collagen deposition (fibrosis), and EMT were investigated. In vitro, human bronchial epithelial (HBE) cells and lung fibroblast cells exposed to the recombinant HB-EGF, collagen deposition and EMT were assessed. We found that sputum HB-EGF expression was significantly increased in patients with COPD compared with non-smokers and smokers without COPD. There was a significant positive correlation between sputum HB-EGF and COPD assessment test (CAT) score. HB-EGF expression was significantly increased in the lung tissue samples of patients with COPD and associated with collagen deposition and N- and E-cadherin, and vimentin expression. In vitro, HB-EGF promoted collagen production in lung fibroblasts. Moreover, HB-EGF induced the EMT process through induction of N-and E-cadherin, and vimentin expression in HBE cells. Collectively, HB-EGF induces airway remodeling by modulating airway fibrosis and pulmonary EMT, and contributes to the COPD severity. The current data may provide insight into the underlying pathogenesis of COPD, in which HB-EGF has an important pathogenic role.
Indexed as
Identifiers
What OpenQuestion holds
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.