Elevated HBP flux in mesangial cells enhances NF-κB transcriptional activity via O-GlcNAc modification, directly upregulating adhesion molecule 1 and amplifying inflammatory signaling through increased NF-κB–DNA binding affinity, sustaining cytokine release and promoting glomerulosclerosis and fibrosis [117, 118]. Here, NFKB1 is linked to glomerulosclerosis.