The aim of this study is to evaluate the role of vimentin in the progression of biliary damage/liver fibrosis and whether there is a mesenchymal phenotype of cholangiocytes in the Mdr2<sup>-/-</sup> model of PSC.
Again, the overexpressed vimentin was observed in the plasma samples derived from patients with hepatic fibrosis/cirrhosis, suggesting that vimentin may be a key factor in regulating the progression of liver fibrosis.
We, for the first time, report the role of WFA in modulating the expression of LOXL2 and Snail1 in addition to vimentin inhibition and regulation of NFκB signaling for the treatment of liver fibrosis.
The goal of this study was to develop a <sup>99m</sup>Tc-labeled N-acetylglucosamine (GlcNAc) that specifically interacts with desmin and vimentin expressed on activated HSCs to monitor the progression and prognosis of liver fibrosis using single-photon emission computed tomography (SPECT) imaging.