ArticleScientific reports2016
Emodin ameliorates bleomycin-induced pulmonary fibrosis in rats by suppressing epithelial-mesenchymal transition and fibroblast activation.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.
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Who cites it
36 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.
- Emodin for pulmonary fibrosis: a systematic review and meta-analysis of efficacy and molecular mechanisms.Frontiers in medicine · 2025Pooled it
- Engineering Resatorvid-Loaded Sub-Microgels of Epigallocatechin-3-gallate/Hyaluronic Acid to Treat Acute Lung Injury.Advanced healthcare materials · 2026Article
- Effects of pirfenidone and fisetin on apoptosis and oxidative stress mechanisms in heart tissue of bleomycin-induced pulmonary fibrosis.Journal of molecular histology · 2026Article
- Chronic Wound Healing: Research Advances from Pathological Mechanisms to Natural Herbal Active Ingredients and Material Delivery Systems.Molecules (Basel, Switzerland) · 2026Review
- Emodin: A Promising Natural Compound for Combating Fibrotic Diseases.Current medical science · 2026Review
- Airway basal stem cell-derived extracellular vesicles modulate proliferation, migration and collagen deposition of fibroblasts.Stem cell research & therapy · 2025Article
- Bone morphogenetic protein 4 ameliorates bleomycin-induced pulmonary fibrosis in mice by repressing NLRP3 inflammasome activation and epithelial-mesenchymal transition.Journal of thoracic disease · 2024Article
- Monomeric compounds from natural products for the treatment of pulmonary fibrosis: a review.Inflammopharmacology · 2024Review
- Combination of Niclosamide and Pirfenidone Alleviates Pulmonary Fibrosis by Inhibiting Oxidative Stress and MAPK/Nf-κB and STATs Regulated Genes.Pharmaceuticals (Basel, Switzerland) · 2023Article
- Utilizing MRI, [Frontiers in nuclear medicine · 2023Article
- Article
- ASK1 Regulates Bleomycin-induced Pulmonary Fibrosis.American journal of respiratory cell and molecular biology · 2022Article
- A Single-Cell Network-Based Drug Repositioning Strategy for Post-COVID-19 Pulmonary Fibrosis.Pharmaceutics · 2022Article
- Effects of bone morphogenetic protein 4 on TGF-PeerJ · 2022Article
- Advances in the study of emodin: an update on pharmacological properties and mechanistic basis.Chinese medicine · 2021Review
- Andrographolide alleviates bleomycin-induced NLRP3 inflammasome activation and epithelial-mesenchymal transition in lung epithelial cells by suppressing AKT/mTOR signaling pathway.Annals of translational medicine · 2021Article
- New Insights into Pathomechanisms and Treatment Possibilities for Lung Silicosis.International journal of molecular sciences · 2021Review
- Protective and therapeutic effects of ethanolic extract ofResearch in pharmaceutical sciences · 2021Article
- Effect of emodin on long non-coding RNA-mRNA networks in rats with severe acute pancreatitis-induced acute lung injury.Journal of cellular and molecular medicine · 2021Article
- Postoperative peritoneal adhesion: an update on physiopathology and novel traditional herbal and modern medical therapeutics.Naunyn-Schmiedeberg's archives of pharmacology · 2021Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aberrant activation of TGF-β1 is frequently encountered and promotes epithelial-mesenchymal transition (EMT) and fibroblast activation in pulmonary fibrosis. The present study investigated whether emodin mediates its effect via suppressing TGF-β1-induced EMT and fibroblast activation in bleomycin (BLM)-induced pulmonary fibrosis in rats. Here, we found that emodin induced apoptosis and inhibited cellular proliferation, migration and differentiation in TGF-β1-stimulated human embryonic lung fibroblasts (HELFs). Emodin suppressed TGF-β1-induced EMT in a dose- and time-dependent manner in alveolar epithelial A549 cells. Emodin also inhibited TGF-β1-induced Smad2, Smad3 and Erk1/2 activation, suggesting that Smad2/3 and Erk1/2 inactivation mediated the emodin-induced effects on TGF-β1-induced EMT. Additionally, we provided in vivo evidence suggesting that emodin apparently alleviated BLM-induced pulmonary fibrosis and improved pulmonary function by inhibiting TGF-β1 signaling and subsequently repressing EMT, fibroblast activation and extracellular matrix (ECM) deposition. Taken together, our data suggest that emodin mediates its effects mainly via inhibition of EMT and fibroblast activation and thus has a potential for the treatment of pulmonary fibrosis.
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Registered trials
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