Taken together, our findings indicate that MFN2 is critical in regulating apoptosis and liver fibrosis in HSCs, which might be a useful therapeutic target to treat liver fibrosis.
Modulation of the Tryptophan Hydroxylase 1/Monoamine Oxidase-A/5-Hydroxytryptamine/5-Hydroxytryptamine Receptor 2A/2B/2C Axis Regulates Biliary Proliferation and Liver Fibrosis During Cholestasis.
The complete absence of IFNγ in Mdr2<sup>-/-</sup>x Ifng<sup>-/-</sup> mice reduced NK cell and CD8<sup>+</sup> T cell frequencies expressing the cytotoxic effector molecules granzyme B and TRAIL and prevented liver fibrosis.
In conclusion, our findings revealed a novel H19/miR-148a/USP4 axis which promoted liver fibrosis via TGF-β pathway in both HSC and hepatocyte, indicating that H19 could become a promising target for the treatment of liver fibrosis.
These results indicate a critical role of OGFRL1 in the mobilization and differentiation of HPC in the fibrotic liver, and administration of OGFRL1-expressing cells may serve as a potential regenerative therapy for advanced liver fibrosis.Stem Cells 2019;37:89-101.
As a recently we developed water-soluble pyridone agent with antifibrotic features, fluorofenidone (AKF-PD) can attenuate liver fibrosis, present studies were designed to explore the role of GSTA3 in liver fibrosis and its modulation by AKF-PD in vivo and in vitro.
Notably, SNHG7 could enhance Wnt/β-catenin pathway activation to contribute to liver fibrosis, with an increase in T cell factor (TCF) activity and a reduction in P-β-catenin level.
<b>Results</b>: Two isoforms of RCAN1 protein were expressed in CCl<sub>4</sub>-induced liver fibrosis mouse model and HSC-T6 cells cultured with transforming growth factor-beta 1 (TGF-β1).
The regulatory subunits of the NOX complex, NCF1 (p47<sup>phox</sup>) and NCF2 (p67<sup>phox</sup>), are up-regulated during HSC activation contributing to ROS production and liver fibrosis.
Moreover, SVIP expression, in agreement with autophagic activity and the volume of lipid droplets, first increases and then decreases during the progression of liver fibrosis with CCl<sub>4</sub> treatment in vivo and in vivo.
This study aimed to explore the therapeutic value of AICAR (5-aminoimidazole-4-carboxyamide ribonucleoside), an agonist of the AMPK pathway, on liver fibrosis and portal hypertension in bile duct ligation (BDL) rats.