LGALS3 promotes liver fibrosis by enhancing the expression and phosphorylation of ERK1/2

To clarify the role of LGALS3 in liver fibrosis, a TGF-β1-induced liver fibrosis model was established, and the expression level of LGALS3 was analyzed. LGALS3 overexpression and knockdown cell lines were constructed in LX-2 cell line. RT-qPCR, western blot, and wound healing assay were employed to investigate the impact of LGALS3 on LX-2 cell activation, proliferation, migration, and the ERK1/2 pathway. In the LGALS3 overexpression cell model, PD98059 intervention was applied to mimic the therapeutic effect on liver fibrosis.​ RESULTS: LGALS3 overexpression significantly promoted the proliferation and migration of LX-2 cells, along with the expression and phosphorylation of ERK1/2. Conversely, LGALS3 knockdown and treatment with the PD98059 inhibitor reduced LX-2 cell proliferation and migration, as well as the phosphorylation of ERK1/2.​ CONCLUSIONS: This study has clarified the pivotal regulatory role of the LGALS3-ERK1/2 signaling axis in liver fibrosis, It reveals that LGALS3 represents a new and promising molecular mechanism that regulates the phosphorylation of ERK1/2. These findings enhance our understanding of the pathological process of liver fibrosis, suggesting that targeting the LGALS3-ERK1/2 axis may represent a promising target for further investigation in liver fibrosis. It also provides potential targets and innovative directions for the development of anti-liver fibrosis drugs.