ArticleProceedings of the American Thoracic Society2008
Escape from the matrix: multiple mechanisms for fibroblast activation in pulmonary fibrosis.
Article in Proceedings of the American Thoracic Society, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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
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
24 citing papers in PubMed, 54 citations in OpenAlex.
- Advancing the understanding of alveolar regeneration: Global research trends, thematic evolution, and emerging frontiers.Regenerative therapy · 2025Review
- A current review on animal models of anti-asthmatic drugs screening.Frontiers in pharmacology · 2025Review
- Comorbidity associated to Ascaris suum infection during pulmonary fibrosis exacerbates chronic lung and liver inflammation and dysfunction but not affect the parasite cycle in mice.PLoS neglected tropical diseases · 2019Article
- The Correlation between Levels of Transforming Growth Factor-β with Pulmonary Fibrosis in Post Pulmonary Tuberculosis in Medan, North Sumatera - Indonesia.Open access Macedonian journal of medical sciences · 2019Article
- Interleukin (IL)-13, Prostaglandin E2 (PGE2), and Prostacyclin 2 (PGI2) Activate Hepatic Stellate Cells via Protein kinase C (PKC) Pathway in Hepatic Fibrosis.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
- ResolvinDLaboratory investigation; a journal of technical methods and pathology · 2018Article
- Lipoxin AERJ open research · 2016Article
- Validated prediction of pro-invasive growth factors using a transcriptome-wide invasion signature derived from a complex 3D invasion assay.Scientific reports · 2015Article
- Lung fibrotic tenascin-C upregulation is associated with other extracellular matrix proteins and induced by TGFβ1.BMC pulmonary medicine · 2014Article
- Regulatory T cells reduce acute lung injury fibroproliferation by decreasing fibrocyte recruitment.American journal of respiratory cell and molecular biology · 2013Article
- Increased survivin expression contributes to apoptosis-resistance in IPF fibroblasts.Advances in bioscience and biotechnology (Print) · 2012Article
- Mechanobiology in lung epithelial cells: measurements, perturbations, and responses.Comprehensive Physiology · 2012Review
- The lens as a model for fibrotic disease.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2011Review
- Idiopathic pulmonary fibrosis-an epidemiological and pathological review.Clinical reviews in allergy & immunology · 2011Review
- TLR9 differentiates rapidly from slowly progressing forms of idiopathic pulmonary fibrosis.Science translational medicine · 2010Article
- Mesenchymal cell survival in airway and interstitial pulmonary fibrosis.Fibrogenesis & tissue repair · 2010Article
- Interstitial lung diseases in children.Orphanet journal of rare diseases · 2010Review
- Signaling pathways in the epithelial origins of pulmonary fibrosis.Cell cycle (Georgetown, Tex.) · 2010Review
- Does chronic microaspiration cause idiopathic pulmonary fibrosis?The American journal of medicine · 2010Review
- Prostaglandin E(2) induces fibroblast apoptosis by modulating multiple survival pathways.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2009Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Lung fibrosis is a recognized feature of many chronic lung diseases and is central to the pathogenesis of idiopathic pulmonary fibrosis, a disease that carries a prognosis worse than many cancers. Current research into this condition is defining the key pathways of activation either in resident fibroblasts, matrix-producing cells derived from circulating fibrocytes, or epithelial cells that appear to transdifferentiate to fibroblast-like cells. The downstream signaling pathways are also being delineated as well as the gene interactions leading to altered cell phenotype. These studies have led to an appreciation that multiple pathways, including inflammatory and coagulation cascades, are involved in the pathogenesis of idiopathic pulmonary fibrosis. As these facts come to light, we are exploring promising new approaches to treat fibroses and halt the inexorable progression that is a feature of these disorders. This article reviews these findings and our current concepts of the key molecular events leading to tissue damage and excessive matrix deposition in lung fibrosis. It also highlights the need for new studies to delineate alternative pathogenetic mechanisms and integrate these pathways so we have a framework to better understand their importance in individual patients.
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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.