Galectin-3 contributes to pathogenesis of IgA nephropathy

Abstract IgA nephropathy (IgAN) is the most common type of autoimmune glomerulonephritis that frequently progresses to end-stage renal disease. However, molecular pathogenesis underlying IgAN remains largely unknown. This study investigated role galectin-3 (Gal-3), a galactoside-binding protein in pathogenesis. Two complementary mouse models, model induced with TEPC-15 hybridoma using Gal-3 knockout (KO) mice, and spontaneous “grouped” ddY (gddY) mice were employed. expression increased disease severity glomeruli, peri-glomerular regions, some tubules both inducible models. KO hybridoma-induced significantly improved proteinuria function reduced pathology, including neutrophil infiltration decreased differentiation Th17 cells from renal-draining lymph nodes, despite percentages regulatory T cells. also inhibited NLRP3 inflammasome, yet it enhanced autophagy inflammation fibrosis. Moreover, administration 6-de-O-sulfated, N-acetylated low-molecular-weight heparin, competitive binding inhibitor, restored lesions passive mice. These results suggest critically involved by activating inflammasome promoting cell differentiation. Therefore, targeting action may represent new therapeutic strategy for treatment this Nil