NDLI: Fedratinib Attenuates Bleomycin-Induced Pulmonary Fibrosis via the JAK2/STAT3 and TGF-β1 Signaling Pathway

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Fedratinib Attenuates Bleomycin-Induced Pulmonary Fibrosis via the JAK2/STAT3 and TGF-β1 Signaling Pathway

Content Provider	MDPI
Author	Ruan, Hao Luan, Jiaoyan Gao, Shaoyan Li, Shuangling Jiang, Qiuyan Liu, Rui Liang, Qing Zhang, Ruiqin Zhang, Fangxia Li, Xiaohe Zhou, Honggang Yang, Cheng
Copyright Year	2021
Description	Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive interstitial lung disease with multiple causes, characterized by excessive myofibrocyte aggregation and extracellular matrix deposition. Related studies have shown that transforming growth factor-β1 (TGF-β1) is a key cytokine causing fibrosis, promoting abnormal epithelial–mesenchymal communication and fibroblast-to-myofibroblast transition. Fedratinib (Fed) is a marketed drug for the treatment of primary and secondary myelofibrosis, targeting selective JAK2 tyrosine kinase inhibitors. However, its role in pulmonary fibrosis remains unclear. In this study, we investigated the potential effects and mechanisms of Fed on pulmonary fibrosis in vitro and in vivo. In vitro studies have shown that Fed attenuates TGF-β1- and IL-6-induced myofibroblast activation and inflammatory response by regulating the JAK2/STAT3 signaling pathway. In vivo studies have shown that Fed can reduce bleomycin-induced inflammation and collagen deposition and improve lung function. In conclusion, Fed inhibited inflammation and fibrosis processes induced by TGF-β1 and IL-6 by targeting the JAK2 receptor.
Starting Page	4491
e-ISSN	14203049
DOI	10.3390/molecules26154491
Journal	Molecules
Issue Number	15
Volume Number	26
Language	English
Publisher	MDPI
Publisher Date	2021-07-26
Access Restriction	Open
Subject Keyword	Molecules Respiratory System Fedratinib Pulmonary Fibrosis Jak2/stat3 Transforming Growth Factor-β1 Fibroblast-to-myofibroblast Transition
Content Type	Text
Resource Type	Article

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