ArticleEMBO molecular medicine2012
Genetic partitioning of interleukin-6 signalling in mice dissociates Stat3 from Smad3-mediated lung fibrosis.
Article in EMBO molecular medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers.
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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.
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Who cites it
85 citing papers in PubMed, 153 citations in OpenAlex.
- Fibroblast growth factor 2 is required for epithelial recovery, but not for pulmonary fibrosis, in response to bleomycin.American journal of respiratory cell and molecular biology · 2015Trial
- Blockade of IL-6 Trans signaling attenuates pulmonary fibrosis.Journal of immunology (Baltimore, Md. : 1950) · 2014Trial
- Interleukin-6 (IL-6) trans signaling drives a STAT3-dependent pathway that leads to hyperactive transforming growth factor-β (TGF-β) signaling promoting SMAD3 activation and fibrosis via Gremlin protein.The Journal of biological chemistry · 2014Trial
- Understanding the Mechanisms Driving Fibrosis Following Cochlear Implantation-Lessons from Other Tissues.Cells · 2025Review
- SHP1 overexpression ameliorates renal fibrosis via inhibition of STAT3 signaling and glycolysis reprogramming.Scientific reports · 2025Article
- Pharmacological inhibition of Epac1 protects against pulmonary fibrosis by blocking FoxO3a neddylation.The European respiratory journal · 2025Article
- Co-culture of human AT2 cells with fibroblasts reveals a MUC5B phenotype: insights from an organoid model.Molecular medicine (Cambridge, Mass.) · 2024Article
- Highly Calibrated Relationship Between Bleomycin Concentrations and Facets of the Active Phase Fibrosis in Classical Mouse Bleomycin Model.International journal of molecular sciences · 2024Article
- Comparison of the Results of Modeling Pulmonary Fibrosis in Sprague Dawley Rats by Intratracheal Administration of Bleomycin in the Form of Sulfate and Chloride at a Dose of 3 mg/kg.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Cellular and Molecular Genetic Mechanisms of Lung Fibrosis Development and the Role of Vitamin D: A Review.International journal of molecular sciences · 2024Review
- Inhibition of STAT3 by S3I-201 suppress peritoneal fibroblast phenotype conversion and alleviate peritoneal fibrosis.Journal of cellular and molecular medicine · 2024Article
- Article
- Treatment of idiopathic pulmonary fibrosis and progressive pulmonary fibrosis: A position statement from the Thoracic Society of Australia and New Zealand 2023 revision.Respirology (Carlton, Vic.) · 2024Article
- JAK/STAT3 signaling in cardiac fibrosis: a promising therapeutic target.Frontiers in pharmacology · 2024Review
- Lung-specific interleukin 6 mediated transglutaminase 2 activation and cardiopulmonary fibrogenesis.Frontiers in immunology · 2024Article
- Perspectives on Post-COVID-19 Pulmonary Fibrosis Treatment.Journal of personalized medicine · 2023Review
- Circadian Disruption in Night Shift Work and Its Association with Chronic Pulmonary Diseases.Advanced biology · 2023Review
- Role of Interleukin-6 Family Cytokines in Organ Fibrosis.Kidney diseases (Basel, Switzerland) · 2023Review
- Exogenous Thymosin Beta 4 Suppresses IPF-Lung Cancer in Mice: Possibly Associated with Its Inhibitory Effect on the JAK2/STAT3 Signaling Pathway.International journal of molecular sciences · 2023Article
- Genetic association of circulating C-reactive protein levels with idiopathic pulmonary fibrosis: a two-sample Mendelian randomization study.Respiratory research · 2023Article
25 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
20 authors at 9 institutions in 4 countries.
Funding
Abstract
Idiopathic pulmonary fibrosis (IPF) is a fatal disease that is unresponsive to current therapies and characterized by excessive collagen deposition and subsequent fibrosis. While inflammatory cytokines, including interleukin (IL)-6, are elevated in IPF, the molecular mechanisms that underlie this disease are incompletely understood, although the development of fibrosis is believed to depend on canonical transforming growth factor (TGF)-β signalling. We examined bleomycin-induced inflammation and fibrosis in mice carrying a mutation in the shared IL-6 family receptor gp130. Using genetic complementation, we directly correlate the extent of IL-6-mediated, excessive Stat3 activity with inflammatory infiltrates in the lung and the severity of fibrosis in corresponding gp130(757F) mice. The extent of fibrosis was attenuated in B lymphocyte-deficient gp130(757F);µMT(-/-) compound mutant mice, but fibrosis still occurred in their Smad3(-/-) counterparts consistent with the capacity of excessive Stat3 activity to induce collagen 1α1 gene transcription independently of canonical TGF-β/Smad3 signalling. These findings are of therapeutic relevance, since we confirmed abundant STAT3 activation in fibrotic lungs from IPF patients and showed that genetic reduction of Stat3 protected mice from bleomycin-induced lung fibrosis.
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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.