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Circulating and Tissue Galectin-3 in Gastrointestinal Inflammation: Clinical Significance and Biomarker Potential
Vesna Brzački1,2, Andriana Jovanović3, Andrija Rančić1
1Gastroenterology and Hepatology Clinic, University Clinical Center Niš, 18000 Niš, Serbia.
Galectin-3 (Gal-3) plays a key role in inflammatory diseases like IBD and liver fibrosis. Inhibiting Gal-3 shows promise in reducing both inflammation and fibrosis, highlighting its therapeutic potential.
Area of Science:
- Immunology
- Molecular Biology
- Cell Biology
Background:
- Galectins are β-galactoside-binding lectins involved in cell interactions.
- Galectin-3 (Gal-3) is multifunctional, found in cytoplasm, nucleus, cell surface, and extracellularly.
- Gal-3 influences immune regulation, fibrosis, and tissue remodeling in various diseases.
Purpose of the Study:
- To explore the role of Galectin-3 in inflammatory conditions.
- To investigate Gal-3's involvement in immune regulation, fibrosis, and tissue remodeling.
- To assess Gal-3 as a potential therapeutic target for inflammatory and fibrotic diseases.
Main Methods:
- Literature review of studies on Galectin-3.
- Analysis of Gal-3 expression and function in inflammatory cells (e.g., macrophages).
- Examination of Gal-3's role in specific diseases like IBD, NASH, and liver fibrosis.
Main Results:
- Gal-3 is implicated in activating the NLRP3 inflammasome, exacerbating intestinal inflammation in IBD.
- Gal-3 promotes fibrosis in liver diseases (PBC, autoimmune hepatitis) via fibroblast activation and ECM deposition.
- Upregulation of Gal-3 in hepatic stellate cells and macrophages contributes to liver fibrosis and inflammation.
Conclusions:
- Galectin-3 is a significant contributor to inflammation and fibrosis in various diseases.
- Targeting Gal-3 demonstrates potential for reducing fibrosis and inflammation.
- Gal-3 inhibition presents a promising therapeutic strategy for inflammatory and fibrotic disorders.
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