AKT1 and diabetic kidney disease: Studies have shown that the significantly elevated O-GlcNAcylation in glomerular mesangial cells can inhibit protein kinase B (AKT) phosphorylation, activate the upstream ASK1 kinase, and promote the phosphorylation of p38 mitogen-activated protein kinase (MAPK), ultimately driving the expression of downstream plasminogen activator inhibitor-l (PAI-1), fibronectin, and transforming growth factor-β1 (TGF-β1), contributing to excessive matrix accumulation in DKD [109, 110].