ArticleJournal of cellular and molecular medicine2020
Emodin inhibiting neutrophil elastase-induced epithelial-mesenchymal transition through Notch1 signalling in alveolar epithelial cells.
Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
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Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.
- The Invasive SpeciesFrontiers in pharmacology · 2022Pooled it
- Next-Generation In Vitro Pulmonary Platforms for Respiratory Disease Modelling and Therapeutic Development: Current Advances and Future Prospects.Medicina (Kaunas, Lithuania) · 2026Review
- Emodin: A Promising Natural Compound for Combating Fibrotic Diseases.Current medical science · 2026Review
- The Immune Microenvironment: New Therapeutic Implications in Organ Fibrosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Sivelestat sodium: a novel therapeutic agent in a mouse model of acute exacerbation pulmonary fibrosis through multiple mechanisms.Journal of thoracic disease · 2025Article
- Exploring the mitigating potential of anthocyanin Malvidin in a mouse model of bleomycin-induced pulmonary fibrosis by inhibiting NLRP3 inflammasome activation and oxidative stress.Journal of inflammation (London, England) · 2025Article
- Epithelial-mesenchymal transition in pulmonary fibrosis: molecular mechanisms and emerging therapeutic strategies.Frontiers in medicine · 2025Review
- A comprehensive review on the cellular mechanism of traditional Chinese medicine in the treatment of pediatric lung diseases.BioImpacts : BI · 2025Review
- Internalisation of neutrophils extracellular traps by macrophages aggravate rheumatoid arthritis via Rab5a.RMD open · 2024Article
- A systematic review of the research progress of traditional Chinese medicine against pulmonary fibrosis: from a pharmacological perspective.Chinese medicine · 2023Review
- The "Elastic Perspective" of SARS-CoV-2 Infection and the Role of Intrinsic and Extrinsic Factors.International journal of molecular sciences · 2022Review
- COX-2/sEH Dual Inhibitor PTUPB Attenuates Epithelial-Mesenchymal Transformation of Alveolar Epithelial CellsOxidative medicine and cellular longevity · 2022Article
- Advances in the study of emodin: an update on pharmacological properties and mechanistic basis.Chinese medicine · 2021Review
- Role of CXCL16 in BLM-induced epithelial-mesenchymal transition in human A549 cells.Respiratory research · 2021Article
- Hindrance of the Proteolytic Activity of Neutrophil-Derived Serine Proteases by Serine Protease Inhibitors as a Management of Cardiovascular Diseases and Chronic Inflammation.Frontiers in chemistry · 2021Review
- Emodin inhibiting neutrophil elastase-induced epithelial-mesenchymal transition through Notch1 signalling in alveolar epithelial cells.Journal of cellular and molecular medicine · 2020Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The transition of alveolar type II epithelial cells into fibroblasts has been reported to cause and/or aggravate pulmonary fibrosis (PF), which is characterized by fibroblast proliferation, an enhanced production and accumulation of ECM (extracellular matrix), alveolar wall damage and functional capillary unit loss. Traditional Chinese medicine Emodin has been reported to inhibit TGF-β-induced epithelial-mesenchymal transition (EMT) in alveolar epithelial cells through Notch signalling. In the present study, neutrophil elastase (NE, also known as ELA2) treatment promoted EMT, Notch1 cleavage (NICD/Notch1 ratio increase) and NICD nuclear translocation in RLE-6TN cells and A549 cells. The promotive roles of NE treatment in these events were significantly reversed by Notch1 knockdown. Traditional Chinese medicine Emodin treatment remarkably inhibited the enzyme activity of NE, suppressed EMT, Notch1 cleavage and NICD nuclear translocation within RLE-6TN and A549 cells, while NE treatment significantly reversed the effects of Emodin. Moreover, in RLE-6TN, the effects of NE on EMT, Notch1 cleavage and NICD nuclear translocation were remarkably attenuated by Emodin treatment and more attenuated by the combination of Emodin and neutrophil elastase inhibitor Sivelestat or notch signal pathway inhibitor DAPT. In conclusion, we revealed the involvement of NE-induced Notch1 cleavage in the functions of Emodin suppressing NE-caused EMT in RLE-6TN cells and A549 cells. This novel mechanism of Emodin inhibiting EMT might extend the application of Emodin in PF treatment.
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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.