Atractylodinol prevents pulmonary fibrosis through inhibiting TGF-β receptor 1 recycling by stabilizing vimentin
文献类型： 外文期刊
作者： Hao, Mengjiao 1 ; Guan, Zhuoji 2 ; Zhang, Zhikang 1 ; Ai, Haopeng 1 ; Peng, Xing 1 ; Zhou, Huihao 1 ; Xu, Jun 1 ; Gu, Qiong 1 ;
作者机构： 1.Sun Yat Sen Univ, Sch Pharmaceut Sci, Guangzhou 510006, Peoples R China
2.Guangzhou Univ Chinese Med, Affiliated Hosp 1, Baiyun Hosp, Guangzhou, Peoples R China
3.Guangdong Acad Agr Sci, Tea Res Inst, Guangdong Key Lab Tea Resources Innovat & Utilizat, Guangzhou 510640, Peoples R China
4.Chinese Acad Sci, Kunming Inst Bot, State Key Lab Phytochemistry & Plant Resources Wes, Kunming 650201, Peoples R China
期刊名称：MOLECULAR THERAPY （ 影响因子：12.4； 五年影响因子：12.6 ）
ISSN： 1525-0016
年卷期： 2023 年 31 卷 10 期
页码：
收录情况： SCI
摘要： Pirfenidone and nintedanib are only anti-pulmonary fibrosis (PF) drugs approved by the FDA. However, they are not target specific, and unable to modify the disease status. Therefore, it is still desirable to discover more effective agents against PF. Vimentin (VIM) plays key roles in tissue regeneration and wound healing, but its molecular mechanism remains unknown. In this work, we demonstrated that atractylodinol (ATD) significantly inhibits TGF-beta 1-induced epithelial-mesenchymal transition and fibroblast-to-myofibroblast transition in vitro. ATD also reduces bleomycin-induced lung injury and fibrosis in mice models. Mechanistically, ATD inhibited TGF-beta receptor I recycling by binding to VIM (K-D = 454 nM) and inducing the formation of filamentous aggregates. In conclusion, we proved that ATD (derived from Atractylodes lancea) modified PF by targeting VIM and inhibiting the TGF-beta/Smad signaling pathway. Therefore, VIM is a druggable target and ATD is a proper drug candidate against PF. We prove a novel VIM function that TGF-beta-receptor I recycling. These findings paved the way to develop new targeted therapeutics against PF.
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