Methylglyoxal is a highly reactive dicarbonyl degradation product formed from triose
phosphates during glycolysis. Methylglyoxal forms stable adducts primarily with arginine
residues of intracellular proteins. The biologic role of this covalent modification in regulating
cell function is not known. Here we report that in mouse kidney endothelial cells, high
glucose causes increased methylglyoxal modification of the corepressor mSin3A.
Methylglyoxal modification of mSin3A results in increased recruitment of O-GlcNAc …