NDLI: Regorafenib-Attenuated, Bleomycin-Induced Pulmonary Fibrosis by Inhibiting the TGF-β1 Signaling Pathway

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Regorafenib-Attenuated, Bleomycin-Induced Pulmonary Fibrosis by Inhibiting the TGF-β1 Signaling Pathway

Content Provider	MDPI
Author	Li, Xiaohe Ma, Ling Huang, Kai Wei, Yuli Long, Shida Liu, Qinyi Zhang, Deqiang Wu, Shuyang Wang, Wenrui Yang, Guang Zhou, Honggang Yang, Cheng
Copyright Year	2021
Description	Idiopathic pulmonary fibrosis (IPF) is a fatal and age-related pulmonary disease. Nintedanib is a receptor tyrosine kinase inhibitor, and one of the only two listed drugs against IPF. Regorafenib is a novel, orally active, multi-kinase inhibitor that has similar targets to nintedanib and is applied to treat colorectal cancer and gastrointestinal stromal tumors in patients. In this study, we first identified that regorafenib could alleviate bleomycin-induced pulmonary fibrosis in mice. The in vivo experiments indicated that regorafenib suppresses collagen accumulation and myofibroblast activation. Further in vitro mechanism studies showed that regorafenib inhibits the activation and migration of myofibroblasts and extracellular matrix production, mainly through suppressing the transforming growth factor (TGF)-β1/Smad and non-Smad signaling pathways. In vitro studies have also indicated that regorafenib could augment autophagy in myofibroblasts by suppressing TGF-β1/mTOR (mechanistic target of rapamycin) signaling, and could promote apoptosis in myofibroblasts. In conclusion, regorafenib attenuates bleomycin-induced pulmonary fibrosis by suppressing the TGF-β1 signaling pathway.
Starting Page	1985
e-ISSN	14220067
DOI	10.3390/ijms22041985
Journal	International Journal of Molecular Sciences
Issue Number	4
Volume Number	22
Language	English
Publisher	MDPI
Publisher Date	2021-02-17
Access Restriction	Open
Subject Keyword	International Journal of Molecular Sciences Immunology Pulmonary Fibrosis Regorafenib Myofibroblasts Tgf-β1 Signaling Pathway
Content Type	Text
Resource Type	Article

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