ArticlePloS one2006
Soluble TNF mediates the transition from pulmonary inflammation to fibrosis.
Article in PloS one, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers, 1 of them a synthesis that pooled it.
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Who cites it
85 citing papers in PubMed, 1 synthesis or guideline pooled it, 135 citations in OpenAlex.
- Toxicity profile of combined immune checkpoint inhibitors and thoracic radiotherapy in esophageal cancer: A meta-analysis and systematic review.Frontiers in immunology · 2022Pooled it
- A tetrahedral framework DNA-based bioswitchable miR-26a-5p delivery system for idiopathic pulmonary fibrosis.Materials today. Bio · 2026Article
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- Variable steady inflammation and inflammatory responses in precision-cut lung slices from various IPF lung Regions.Respiratory research · 2025Article
- Taiwan Chingguan Yihau may improve post-COVID-19 respiratory complications through PI3K/AKT, HIF-1, and TNF signaling pathways revealed by network pharmacology analysis.Molecular diversity · 2025Article
- Inhibition of Talin2 dedifferentiates myofibroblasts and reverses lung and kidney fibrosis.Scientific reports · 2025Article
- Overlapping Systemic Proteins in COVID-19 and Lung Fibrosis Associated with Tissue Remodeling and Inflammation.Biomedicines · 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
- Blocking antibodies against integrin-α3, -αM, and -αMβ2 de-differentiate myofibroblasts, and improve lung fibrosis and kidney fibrosis.Scientific reports · 2024Article
- TGF-β1 Drives Integrin-Dependent Pericyte Migration and Microvascular Destabilization in Fibrotic Disease.The American journal of pathology · 2024Article
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- Targeting Tumor Necrosis Factor Alpha to Mitigate Lung Injury Induced by Mustard Vesicants and Radiation.Disaster medicine and public health preparedness · 2023Review
- Apoptotic cell death in disease-Current understanding of the NCCD 2023.Cell death and differentiation · 2023Review
- Increased lipocalin-2 expression in pulmonary inflammation and fibrosis.Frontiers in medicine · 2023Article
- TNF superfamily control of tissue remodeling and fibrosis.Frontiers in immunology · 2023Review
- Blockade of the pentraxin 3/CD44 interaction attenuates lung injury-induced fibrosis.Clinical and translational medicine · 2022Article
- Association of TNF-α, TGF-β1, amphiregulin, IL-2, and EGFR WITH pulmonary fibrosis in COVID-19.Journal of infection and public health · 2022Article
- Targeted proteomics identifies circulating biomarkers associated with active COVID-19 and post-COVID-19.Frontiers in immunology · 2022Article
- Plant polysaccharides with anti-lung injury effects as a potential therapeutic strategy for COVID-19.Frontiers in pharmacology · 2022Review
- Prevention of mortality in acute lung injury induced by oleic acid: Application of polyherbal decoction (bronco T).Frontiers in cell and developmental biology · 2022Article
25 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
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundFibrosis, the replacement of functional tissue with excessive fibrous tissue, can occur in all the main tissues and organ systems, resulting in various pathological disorders. Idiopathic Pulmonary Fibrosis is a prototype fibrotic disease involving abnormal wound healing in response to multiple sites of ongoing alveolar epithelial injury. METHODOLOGY/PRINCIPAL
findingsTo decipher the role of TNF and TNF-mediated inflammation in the development of fibrosis, we have utilized the bleomycin-induced animal model of Pulmonary Fibrosis and a series of genetically modified mice lacking components of TNF signaling. Transmembrane TNF expression is shown to be sufficient to elicit an inflammatory response, but inadequate for the transition to the fibrotic phase of the disease. Soluble TNF expression is shown to be crucial for lymphocyte recruitment, a prerequisite for TGF-b1 expression and the development of fibrotic lesions. Moreover, through a series of bone marrow transfers, the necessary TNF expression is shown to originate from the non-hematopoietic compartment further localized in apoptosing epithelial cells.
conclusionsThese results suggest a primary detrimental role of soluble TNF in the pathologic cascade, separating it from the beneficial role of transmembrane TNF, and indicate the importance of assessing the efficacy of soluble TNF antagonists in the treatment of Idiopathic Pulmonary Fibrosis.
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