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Author Spotlight: Investigating the Potential of Chinese Herbal Medicinal Active Dioscin in Treating IgA Nephropathy
Published on: October 13, 2023
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Galectin-3 contributes to pathogenesis of IgA nephropathy
Yu-Ling Chou1, Hung-Lin Chen2, Bang-Gee Hsu3
1Graduate Institute of Life Sciences, National Defense Medical Center, Taipei, Taiwan.
Kidney International
|July 31, 2024
Summary
Galectin-3 (Gal-3) plays a key role in IgA nephropathy (IgAN) progression. Inhibiting Gal-3 improves kidney function and reduces inflammation in IgAN models, suggesting it as a potential therapeutic target.
Area of Science:
- Nephrology
- Immunology
- Molecular Biology
Background:
- IgA nephropathy (IgAN) is a leading cause of kidney failure, but its molecular mechanisms are poorly understood.
- Galectin-3 (Gal-3), a galactoside-binding protein, has been implicated in various inflammatory conditions.
Purpose of the Study:
- To investigate the role of Gal-3 in the pathogenesis of IgA nephropathy (IgAN).
- To explore Gal-3 as a potential therapeutic target for IgAN.
Main Methods:
- Examined Gal-3 expression in IgAN patient kidneys and mouse models.
- Utilized Gal-3 knockout mice and a Gal-3 binding inhibitor in passive IgAN models.
- Assessed kidney function, pathology, immune cell differentiation, inflammasome activity, and autophagy.
Main Results:
- Gal-3 expression was significantly elevated in IgAN kidneys and correlated with disease severity.
- Gal-3 knockout mice showed reduced proteinuria, improved kidney function, and attenuated kidney pathology.
- Gal-3 inhibition decreased Th17 cell differentiation, suppressed NLRP3 inflammasome activation, enhanced autophagy, and reduced kidney inflammation and fibrosis.
Conclusions:
- Gal-3 is critically involved in IgAN pathogenesis.
- Targeting Gal-3 action, potentially with inhibitors, offers a promising new therapeutic strategy for IgAN treatment.
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