ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2012
Galectin-3 modulates phagocytosis-induced stellate cell activation and liver fibrosis in vivo.
Article in American journal of physiology. Gastrointestinal and liver physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 86 citations in OpenAlex.
- The Sugar-Coated Truth of Alcohol-Associated Liver Disease: Galectins as Multifaceted Regulators of Alcohol-Induced Liver Injury.The American journal of pathology · 2026Review
- LGALS3 marks a pro-inflammatory, efferocytosis-low hepatic macrophage state and promotes hepatic stellate cell activation through the candidate receptor ANXA2 in liver cirrhosis.Frontiers in immunology · 2026Article
- The Role of Galectin-3 in Liver Inflammation and Fibrosis.Journal of inflammation research · 2026Review
- Review
- Hepatic stellate cell inhibition by angiotensin II receptor blocker mitigates liver injury and fibrosis via NF-κB-galectin-3 suppression in a rat nonalcoholic steatohepatitis model.Archives of toxicology · 2025Article
- Exploring the impact of galectins on liver cancer: From immunopathogenesis to potential targets.World journal of gastroenterology · 2025Review
- Therapeutic Strategies for MASH: An Update on Drug Candidates Under Investigation in Late-Phase Clinical Trials.International journal of translational medicine (Basel, Switzerland) · 2025Article
- Current Therapeutic Landscape for Metabolic Dysfunction-Associated Steatohepatitis.International journal of molecular sciences · 2025Review
- Galectins and Liver Diseases.International journal of molecular sciences · 2025Review
- ECM remodeling in hypothyroidism-associated MAFLD: mechanisms, clinical relevance, and therapeutic targets.Frontiers in immunology · 2025Review
- Review
- Galectin-3 in biliary atresia and other pediatric cholestatic liver diseases.Hepatology research : the official journal of the Japan Society of Hepatology · 2024Article
- The role of macrophages in liver fibrosis: composition, heterogeneity, and therapeutic strategies.Frontiers in immunology · 2024Review
- Efferocytosis in liver disease.JHEP reports : innovation in hepatology · 2024Review
- Galectin-3 and Severity of Liver Fibrosis in Metabolic Dysfunction-Associated Fatty Liver Disease.Protein and peptide letters · 2024Review
- Secretory GFP reconstitution labeling of neighboring cells interrogates cell-cell interactions in metastatic niches.Nature communications · 2023Article
- Intermittent Fasting Attenuates Metabolic-Dysfunction-Associated Steatohepatitis by Enhancing the Hepatic Autophagy-Lysosome Pathway.Nutrients · 2023Article
- Identification of LBH and SPP1 involved in hepatic stellate cell activation during liver fibrogenesis.Human cell · 2023Article
- Development of Galectin-3 Targeting Drugs for Therapeutic Applications in Various Diseases.International journal of molecular sciences · 2023Review
- Increased Expression of Galectin-3 in Skin Fibrosis: Evidence from In Vitro and In Vivo Studies.International journal of molecular sciences · 2022Article
Corrections and comments
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Authors and funding
14 authors at 3 institutions in 2 countries.
Funding
Abstract
Hepatic stellate cells (HSC), the key fibrogenic cells of the liver, transdifferentiate into myofibroblasts upon phagocytosis of apoptotic hepatocytes. Galectin-3, a β-galactoside-binding lectin, is a regulator of the phagocytic process. In this study, our aim was to study the mechanism by which extracellular galectin-3 modulates HSC phagocytosis and activation. The role of galectin-3 in engulfment was evaluated by phagocytosis and integrin binding assays in primary HSC. Galectin-3 expression was studied by real-time PCR and enzyme-linked immunosorbent assay, and in vivo studies were done in wild-type and galectin-3(-/-) mice. We found that HSC from galectin-3(-/-) mice displayed decreased phagocytic activity, expression of transforming growth factor-β1, and procollagen α1(I). Recombinant galectin-3 reversed this defect, suggesting that extracellular galectin-3 is required for HSC activation. Galectin-3 facilitated the α(v)β(3) heterodimer-dependent binding, indicating that galectin-3 modulates HSC phagocytosis via cross-linking this integrin and enhancing the tethering of apoptotic cells. Blocking integrin α(v)β(3) resulted in decreased phagocytosis. Galectin-3 expression and release were induced in active HSC engulfing apoptotic cells, and this was mediated by the nuclear factor-κB signaling. The upregulation of galectin-3 in active HSC was further confirmed in vivo in bile duct-ligated (BDL) rats. Galectin-3(-/-) mice displayed significantly decreased fibrosis, with reduced expression of α-smooth muscle actin and procollagen α1(I) following BDL. In summary, extracellular galectin-3 plays a key role in liver fibrosis by mediating HSC phagocytosis, activation, and subsequent autocrine and paracrine signaling by a feedforward mechanism.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.