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Different effects of growth factors on proliferation and matrix production of normal and fibrotic human lung fibroblasts.
Review in Lung. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers.
What it found
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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
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Who cites it
90 citing papers in PubMed, 181 citations in OpenAlex.
- Transcriptomic signatures of IPF in ALI-cultured airway cells and their therapeutic implications.Thorax · 2026Article
- Optimization of serum-free medium supplemented with microalgal extract using response surface methodology for human fibroblast culture.Journal of biological engineering · 2026Article
- Biomarkers of pulmonary fibrosis in bronchoalveolar lavage fluid and saliva. Study methods and pathophysiological significance.Frontiers in medicine · 2026Review
- Reprogrammed Fibrotic Niche Fuels Lung Cancer Initiation and Reciprocal Remodeling.International journal of biological sciences · 2026Review
- Large scale plasma proteomic profiles improve prediction of idiopathic pulmonary fibrosis in general population.Respiratory research · 2025Article
- Clonal expansion of alveolar fibroblast progeny drives pulmonary fibrosis in mouse models.The Journal of clinical investigation · 2025Article
- A bio-inspired screwed small-diameter vascular graft for endotheliazation and arterial regeneration.Bioactive materials · 2025Article
- miR-146b disrupts the epidermal growth factor receptor/transforming growth factor β receptor profibrotic feedforward loop to inhibit lung fibroblast proliferation and differentiation.The Journal of pharmacology and experimental therapeutics · 2025Article
- The growth hormone/IGF-1 axis is a risk factor for long-term kidney allograft failure.JCI insight · 2025Article
- Fibrosis in PCLS: comparing TGF-β and fibrotic cocktail.Respiratory research · 2025Article
- Inhalable Carbonyl Sulfide Donor-Hybridized Selective Phosphodiesterase 10A Inhibitor for Treating Idiopathic Pulmonary Fibrosis by Inhibiting Tumor Growth Factor-β Signaling and Activating the cAMP/Protein Kinase A/cAMP Response Element-Binding Protein (CREB)/p53 Axis.ACS pharmacology & translational science · 2025Article
- Mechanical stretch-induced IGF2 overexpression in epidermal keratinocytes promotes hypertrophic scar formation through the IGF1R/p-c-Jun axis.International journal of biological sciences · 2025Article
- Article
- Characterization of dental dust particles and their pathogenicity to respiratory system: a narrative review.Clinical oral investigations · 2023Review
- Pulmonary Fibrosis as a Result of Acute Lung Inflammation: Molecular Mechanisms, Relevant In Vivo Models, Prognostic and Therapeutic Approaches.International journal of molecular sciences · 2022Review
- Insulin-like Growth Factor-2 (IGF-2) in Fibrosis.Biomolecules · 2022Review
- Targeting Growth Factor and Cytokine Pathways to Treat Idiopathic Pulmonary Fibrosis.Frontiers in pharmacology · 2022Review
- Dysregulated overexpression of Sox9 induces fibroblast activation in pulmonary fibrosis.JCI insight · 2021Article
- Immune Stroma in Lung Cancer and Idiopathic Pulmonary Fibrosis: A Common Biologic Landscape?International journal of molecular sciences · 2021Review
- Emerging cellular and molecular determinants of idiopathic pulmonary fibrosis.Cellular and molecular life sciences : CMLS · 2021Review
30 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
OBJECTIVES AND
methodsIn idiopathic pulmonary fibrosis (IPF), proliferation of fibroblasts and increased matrix deposition result in pulmonary damage and respiratory insufficiency. We cultured human fibroblasts from lung biopsies of healthy adults and of three patients with IPF (histologically usual interstital pneumonitis, UIP) in order to compare proliferation ([(3)H]thymidine incorporation, cell count) and matrix protein expression (immune fluorescence, quantification of fibronectin synthesis using time-resolved immune fluorescence) of normal and UIP fibroblasts in response to various growth factors.
findingsThe growth factors platelet-derived growth factor-BB (PDGF), epidermal growth factor (EGF), insulin growth factor-1 (IGF-1), insulin-like growth factor-2 (IGF-2), tumor necrosis factor alpha (TNFalpha), Transforming growth factor-beta (TGFbeta(1)), and fibroblast growth factor-2 (FGF-2) stimulate proliferation of normal lung fibroblasts significantly more than proliferation of UIP fibroblasts. Immunofluorescence reveals extensive expression of collagen I, collagen III, and fibronectin induced by serum, TGFbeta(1), and TNFalpha. This expression is more pronounced in UIP fibroblasts than in normal fibroblasts. Quantification of fibronectin synthesis reveals an enhanced fibronectin synthesis by UIP fibroblasts in response to PDGF, EGF, IGF-1, IGF-2, TNFalpha, TGFbeta(1), and FGF-2).
conclusionsFibroblasts from normal and UIP lungs differ in their response to growth factors: Whereas normal fibroblasts show a predominantly proliferative response, UIP fibroblasts show an enhanced synthetic activity. Different fibroblast responses may contribute to progressive pulmonary fibrosis in patients with UIP.
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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.