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.
In addition, we found that hBM-MSCs-Ex inhibited the expression of Wnt/β-catenin pathway components (PPARγ, Wnt3a, Wnt10b, β-catenin, WISP1, Cyclin D1), α-SMA, and Collagen I, in both HSCs and liver fibrosis tissue.
In this review, we present recent insights into the correlation between Wnt/β-catenin signaling and liver fibrosis and discuss the antifibrotic effects of the cAMP-response element binding protein/β-catenin inhibitor PRI-724.
In conclusion, the present study demonstrated that NOR1 activates HSCs and contributes to liver fibrosis in vitro and this effect was achieved through the activation of the Wnt/β‑catenin pathway.
Aberrant activated Wnt/β-catenin pathway is known to accelerate the development of liver fibrosis. microRNAs (miRNAs)-mediated Wnt/β-catenin pathway has been reported to be involved in HSC activation during liver fibrosis.
In this study, we examined the expression of lncRNA-ATB/miR-200a, and their target gene β-Catenin in liver tissues of HCV patients and hepatic stellate cells (HSCs) to elucidate the possible role of lncRNA-ATB/miR-200a axis in HSC activation and development of liver fibrosis.