10.6084/m9.figshare.5241841.v1 Kim M.-J. Kim M.-J. Park S.-A. Park S.-A. Kim C.H. Kim C.H. Park S.-Y. Park S.-Y. Kim J.-S. Kim J.-S. Kim D.-K. Kim D.-K. Nam J.-S. Nam J.-S. Sheen Y.Y. Sheen Y.Y. Erratum: TGF-β Type I Receptor Kinase Inhibitor EW-7197 Suppresses Cholestatic Liver Fibrosis by Inhibiting HIF1α-Induced Epithelial Mesenchymal Transition Karger Publishers 2017 Cholestatic liver injury Hepatic stellate cell TGF-β HIF1α Epithelial mesenchymal transition EW-7197 2017-07-25 13:58:49 Dataset https://karger.figshare.com/articles/dataset/Erratum_TGF-_Type_I_Receptor_Kinase_Inhibitor_EW-7197_Suppresses_Cholestatic_Liver_Fibrosis_by_Inhibiting_HIF1_-Induced_Epithelial_Mesenchymal_Transition/5241841 <b><i>Background/Aims: </i></b>Hypoxia is an environmental factor that aggravates liver fibrosis. HIF1α activates hepatic stellate cells (HSCs) and increases transforming growth factor-β (TGF-β) signaling and the epithelial mesenchymal transition (EMT), accelerating the progression of fibrosis. We evaluated the anti-fibrotic therapeutic potential of a small-molecule inhibitor of TGF-β type I receptor kinase, EW-7197, on HIF1α-derived TGF-β signaling in cholestatic liver fibrosis. <b><i>Methods: </i></b>We used a bile duct ligation (BDL)-operated rat model to characterize the role of HIF1α-derived TGF-β signaling in liver fibrosis. Cellular assays were performed in LX-2 cells (human immortalized HSCs). The anti-fibrotic effects of EW-7197 in liver tissues and HSCs were investigated via biochemical assays, immunohistochemistry (IHC), immunofluorescence (IF), chromatin immunoprecipitation (ChIP) assays, real-time PCR, and western blotting. <b><i>Results: </i></b>In our BDL rat model, orally administered EW-7197 inhibited fibrosis and attenuated HIF1α-induced activation of HSCs and EMT <i>in vivo</i>. In addition, EW-7197 inhibited HIF1α-derived HSC activation and expression of EMT markers in LX-2 cells <i>in vitro. </i><b><i>Conclusion: </i></b>This study suggests that EW-7197 exhibits potential as a treatment for liver fibrosis because it inhibits HIF1α-induced TGF-β signaling.