ArticleDrug design, development and therapy2020
Tranilast Inhibits Pulmonary Fibrosis by Suppressing TGFβ/SMAD2 Pathway.
Article in Drug design, development and therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 26 citations in OpenAlex.
- Epithelial Cell Dysfunction in Pulmonary Fibrosis: Mechanisms, Interactions, and Emerging Therapeutic Targets.Pharmaceuticals (Basel, Switzerland) · 2025Review
- The role of vascularity and the fibrovascular interface in interstitial lung diseases.European respiratory review : an official journal of the European Respiratory Society · 2025Review
- Unlocking the potential of tranilast: Targeting fibrotic signaling pathways for therapeutic benefit.International immunopharmacology · 2024Review
- Pyroptosis in renal inflammation and fibrosis: current knowledge and clinical significance.Cell death & disease · 2023Review
- Polydopamine-assisted tranilast immobilization on a PLA chamber to enhance fat flaps regeneration by reducing tissue fibrosis.RSC advances · 2023Article
- Mechanisms of NLRP3 inflammasome-mediated hepatic stellate cell activation: Therapeutic potential for liver fibrosis.Genes & diseases · 2023Review
- Tranilast attenuates lipopolysaccharide‑induced lung injury via the CXCR4/JAK2/STAT3 signaling pathway.Molecular medicine reports · 2022Article
- Asthma and Post-Asthmatic Fibrosis: A Search for New Promising Molecular Markers of Transition from Acute Inflammation to Pulmonary Fibrosis.Biomedicines · 2022Article
- The Mechanism and Regulation of the NLRP3 Inflammasome during Fibrosis.Biomolecules · 2022Review
- Tranilast inhibits angiotensin II-induced myocardial fibrosis through S100A11/ transforming growth factor-β (TGF-β1)/Smad axis.Bioengineered · 2021Article
- Article
- Tranilast: a potential anti-Inflammatory and NLRP3 inflammasome inhibitor drug for COVID-19.Immunopharmacology and immunotoxicology · 2021Review
Corrections and comments
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Authors and funding
18 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeIdiopathic pulmonary fibrosis (IPF) is characterized by the accumulation of extracellular matrix (ECM) protein in the lungs. Transforming growth factor (TGF) β-induced ECM protein synthesis contributes to the development of IPF. Tranilast, an anti-allergy drug, suppresses TGFβ expression and inhibits interstitial renal fibrosis in animal models. However, the beneficial effects of tranilast or its mechanism as a therapy for pulmonary fibrosis have not been clarified.
methodsWe investigated the in vitro effect of tranilast on ECM production and TGFβ/SMAD2 pathway in TGFβ2-stimulated A549 human alveolar epithelial cells, using quantitative polymerase chain reaction, Western blotting, and immunofluorescence. In vitro observations were validated in the lungs of a murine pulmonary fibrosis model, which we developed by intravenous injection of bleomycin.
resultsTreatment with tranilast suppressed the expression of ECM proteins, such as fibronectin and type IV collagen, and attenuated SMAD2 phosphorylation in TGFβ2-stimulated A549 cells. In addition, based on a wound healing assay in these cells, tranilast significantly inhibited cell motility, with foci formation that comprised of ECM proteins. Histological analyses revealed that the administration of tranilast significantly attenuated lung fibrosis in mice. Furthermore, tranilast treatment significantly reduced levels of TGFβ, collagen, fibronectin, and phosphorylated SMAD2 in pulmonary fibrotic tissues in mice.
conclusionThese findings suggest that tranilast inhibits pulmonary fibrosis by suppressing TGFβ/SMAD2-mediated ECM protein production, presenting tranilast as a promising and novel anti-fibrotic agent for the treatment of IPF.
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