ArticleEuropean journal of medical research2025
LGALS3 promotes liver fibrosis by enhancing the expression and phosphorylation of ERK1/2.
Article in European journal of medical research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- The Role of Galectin-3 in Liver Inflammation and Fibrosis.Journal of inflammation research · 2026Review
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5 authors.
Funding
Abstract
backgroundLiver fibrosis represents the common endpoint of numerous chronic liver diseases. Current therapeutic approaches predominantly focus on alleviating symptoms or addressing the underlying causes, with limited options available for reversing fibrosis. Existing antifibrotic drugs often exhibit low efficacy and carry significant side effects, underscoring the urgent need for novel therapeutic targets. LGALS3, a β-galactoside-binding lectin, participates in inflammation and fibrosis across multiple organs. However, its specific role in liver fibrosis remains poorly understood. This study endeavors to elucidate the cellular and molecular mechanisms by which LGALS3 regulates liver fibrosis and assess its potential as a therapeutic target. SUBJECTS AND
methodsTo 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.
resultsLGALS3 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.
conclusionsThis 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.
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