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Amiodarone is a high effectiveness anti-arrhythmia agent which is able to induce pulmonary fibrosis. Many studies have shown that the epithelial-mesenchymal transition (EMT) was a significant process in pulmonary fibrosis. So far, there are no studies about whether EMT was associated with amiodarone-induced pulmonary fibrosis, which was therefore explored in this study. In addition, the underlying mechanisms of amiodarone-induced pulmonary fibrosis were examined in vitro. We found the EMT marker (α-SMA) was significantly increased, while the E-cadherin was significantly decreased in adenocarcinomic human alveolar basal epithelial cells (A549) after amiodarone treatment, suggesting that the epithelial cells were an important source of mesenchymal cells. Transforming growth factor beta1 (TGF-β1) was also increased significantly after amiodarone treatment. In conclusion, this study suggested amiodarone could induce pulmonary fibrosis via EMT, and the TGF-β1 may be a key profibrotic cytokine in mechanisms of amiodarone-induced pulmonary fibrosis.


Jie Weng, Hao Chen, He Wu, Mengyun Tu, Zhibin Wang, Daqing Chen, Zhiyi Wang, Chan Chen. Amiodarone induces epithelial-mesenchymal transition in A549 cells via activation of TGF-β1. Drug and chemical toxicology. 2020 Jul;43(4):415-422

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PMID: 30192650

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