Aberrant Glycosylation Drives Kidney Disease Pathogenesis. (IMAGE)
Caption
Aberrant Glycosylation Drives Kidney Disease Pathogenesis. This schematic illustrates how abnormal glycosylation contributes to diverse kidney diseases: (A) galactose-deficient IgA1 in Henoch–Schönlein purpura nephritis, (B) IgG4 glycosylation defects in primary membranous nephropathy, (C) N-glycosylation changes in anti-GBM disease, (D) altered IgG glycosylation in lupus nephritis, and (E) polycystin glycosylation defects in autosomal dominant polycystic kidney disease. These molecular changes disrupt immune regulation, protein stability, and signaling pathways, driving renal inflammation, fibrosis, and structural injury.
Credit
Precision Clinical Medicine
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