ArticleScientific reports2017
Thalidomide Inhibits TGF-β1-induced Epithelial to Mesenchymal Transition in Alveolar Epithelial Cells via Smad-Dependent and Smad-Independent Signaling Pathways.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 36 citations in OpenAlex.
- Targeting fibrosis in the treatment of lower urinary tract dysfunction.The Journal of pathology · 2026Article
- Idiopathic Pulmonary Fibrosis, Today and Tomorrow: Certainties and New Therapeutic Horizons.Pulmonary therapy · 2025Review
- Drugs targeting CTGF in the treatment of pulmonary fibrosis.Journal of cellular and molecular medicine · 2024Review
- The Plastic Interplay between Lung Regeneration Phenomena and Fibrotic Evolution: Current Challenges and Novel Therapeutic Perspectives.International journal of molecular sciences · 2023Review
- Respiratory Syncytial Virus Infection Does Not Induce Epithelial-Mesenchymal Transition.Journal of virology · 2023Article
- Amphiregulin induces CCN2 and fibronectin expression by TGF-β through EGFR-dependent pathway in lung epithelial cells.Respiratory research · 2022Article
- Meleagrin Isolated from the Red Sea FungusBiomedicines · 2022Article
- Idiopathic pulmonary fibrosis: Current and future treatment.The clinical respiratory journal · 2022Review
- Phosphate Toxicity and Epithelial to Mesenchymal Transition.Advances in experimental medicine and biology · 2022Article
- Shenkang Injection for Treating Renal Fibrosis-Metabonomics and Regulation of E3 Ubiquitin Ligase Smurfs on TGF-β/Smads Signal Transduction.Frontiers in pharmacology · 2022Article
- Isotretinoin and Thalidomide Down-RegulateMolecules (Basel, Switzerland) · 2021Article
- Emerging cellular and molecular determinants of idiopathic pulmonary fibrosis.Cellular and molecular life sciences : CMLS · 2021Review
- Application of Histone Deacetylase Inhibitors in Renal Interstitial Fibrosis.Kidney diseases (Basel, Switzerland) · 2020Review
- Astragaloside IV attenuates high glucose-induced EMT by inhibiting the TGF-β/Smad pathway in renal proximal tubular epithelial cells.Bioscience reports · 2020Article
- Dual role of RACK1 in airway epithelial mesenchymal transition and apoptosis.Journal of cellular and molecular medicine · 2020Article
- Epithelial mesenchymal transition (EMT): a universal process in lung diseases with implications for cystic fibrosis pathophysiology.Respiratory research · 2018Review
- MEIS-1 level in unresectable hepatocellular carcinoma can predict the post-treatment outcomes of radiofrequency ablation.Oncotarget · 2018Article
- PAK4 enhances TGF-β1-induced epithelial-mesenchymal transition through activating β-catenin signaling pathway in renal tubular epithelial cells.International journal of clinical and experimental pathology · 2018Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent evidence indicates that the epithelial to mesenchymal transition (EMT) in primary alveolar cells (AECs) plays an important role in idiopathic pulmonary fibrosis (IPF). In vivo models have suggested that thalidomide (THL) has anti-fibrotic effects against pulmonary fibrosis, but the underlying mechanism of this effect is not clear. This study investigated whether THL regulates alveolar EMT and the possible mechanisms underlying this process. CCL-149 cells were treated with TGF-β1 in the presence of THL at the indicated concentrations. EMT was assessed by changes in cell morphology and in phenotypic markers. Signaling pathways involved in EMT were characterized by western blot analysis. THL inhibited the TGF-β1 induction of α-SMA, vimentin, MMP-2/-9 and collagen type IV expression and restored the morphological changes in primary alveolar epithelial cells caused by TGF-β1. TGF-β1 induction of α-SMA expression was partially dependent on the activation of p38, JNK, ERK, Akt, Smad 2 and Smad3. Moreover, THL inhibited TGF-β1-induced phosphorylation of p38, JNK, ERK, Akt, GSK3β, Smad 2 and Smad3 without altering the total expression levels of those proteins. These findings indicate that TGF-β1-induced EMT in alveolar epithelial cells is inhibited by THL via both Smad-dependent and non-Smad-dependent signaling pathways and suggests therapeutic approaches for targeting this process in pulmonary fibrosis.
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