ArticleThe Journal of pathology2017
Fibroblast growth factors and pulmonary fibrosis: it's more complex than it sounds.
Article in The Journal of pathology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 33 citations in OpenAlex.
- A FGFR3 decoy receptor attenuates lung fibroblast-to-myofibroblast transition and pulmonary fibrosis.American journal of respiratory cell and molecular biology · 2026Article
- Review
- Nintedanib increases BCL-2 in fibrotic fibroblasts, enhancing ABT-199 apoptosis and fibrosis resolution.American journal of respiratory cell and molecular biology · 2026Article
- A comprehensive review on the cellular mechanism of traditional Chinese medicine in the treatment of pediatric lung diseases.BioImpacts : BI · 2025Review
- Lung-gut axis, intestinal microbiota, and pulmonary fibrosis: mechanisms and therapeutic potential.Frontiers in microbiology · 2025Review
- Senescent lung-resident mesenchymal stem cells drive pulmonary fibrogenesis through FGF-4/FOXM1 axis.Stem cell research & therapy · 2024Article
- Systems-based identification of the Hippo pathway for promoting fibrotic mesenchymal differentiation in systemic sclerosis.Nature communications · 2024Article
- Inhibition of discoidin domain receptor 2 reveals kinase-dependent and kinase-independent functions in regulating fibroblast activity.American journal of physiology. Lung cellular and molecular physiology · 2023Article
- A systematic review of the research progress of traditional Chinese medicine against pulmonary fibrosis: from a pharmacological perspective.Chinese medicine · 2023Review
- Dynamic atlas of immune cells reveals multiple functional features of macrophages associated with progression of pulmonary fibrosis.Frontiers in immunology · 2023Article
- Association of fibroblast growth factor 10 with the fibrotic and inflammatory pathogenesis of Graves' orbitopathy.PloS one · 2021Article
- MiR-503 suppresses fibroblast activation and myofibroblast differentiation by targeting VEGFA and FGFR1 in silica-induced pulmonary fibrosis.Journal of cellular and molecular medicine · 2020Article
- Type I Collagen Signaling Regulates Opposing Fibrotic Pathways through αAmerican journal of respiratory cell and molecular biology · 2020Article
- Diverse Injury Pathways Induce Alveolar Epithelial Cell CCL2/12, Which Promotes Lung Fibrosis.American journal of respiratory cell and molecular biology · 2020Article
- Transforming growth factor β1 alters the 3'-UTR of mRNA to promote lung fibrosis.The Journal of biological chemistry · 2019Article
- Developmental pathways in the pathogenesis of lung fibrosis.Molecular aspects of medicine · 2019Review
- Fine-tuning the ubiquitin-proteasome system to treat pulmonary fibrosis.Connective tissue research · 2019Review
- FGF-2 inhibits contractile properties of valvular interstitial cell myofibroblasts encapsulated in 3D MMP-degradable hydrogels.APL bioengineering · 2018Article
- The chemokines CXCL12 and CXCL14 differentially regulate connective tissue markers during limb development.Scientific reports · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Lung fibrosis results from the cumulative effect of dysfunctional wound repair involving multiple cell types, including fibroblasts, epithelial cells, and macrophages responding to an array of soluble and matrix-mediated stimuli. Recent studies have shown that a tyrosine kinase inhibitor that targets FGF, VEGF, and PDGF receptors can slow the rate of decline in pulmonary function in patients with idiopathic pulmonary fibrosis. However, each of these growth factor families is comprised of multiple ligands and receptors with pleiotropic activities on different cell types such that their broad inhibition might have both pro-fibrotic and anti-fibrotic effects, limiting the potential therapeutic efficacy. Continued investigation and delineation of specific roles of individual proteins and receptors on different cell types hold promise for targeting specific pathways with precision and optimizing the potential efficacy of future approaches to lung fibrosis therapy. Copyright © 2016 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
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.