Role of glycolysis in diabetic atherosclerosis

Figure 1 Effects of glycolysis on endothelial cells in hyperglycemic environment. The activity of glucose transporter 1 is regulated by extracellular glucose concentration, independent of insulin, making endothelial cells in patients with diabetes more vulnerable. Nitrosation stress caused by diabetes can damage DNA and activate poly polymerase 1 (PARP1). PARP1 can not only promote the consumption of NAD+, but also reduce the activity of GAPDH after adenosine diphosphate ribosylation. Both pathways inhibit glycolysis and lead to dysfunction of ECs. Diabetes can promote the accumulation of advanced glycosylation end-products (AGEs), and diabetes-induced reactive oxygen species can increase the expression of receptor for AGE and pro-inflammatory endogenous ligands. The above process leads to the down-regulation of ECs glycolysis and the intensification of inflammation, causing decreased migration and proliferation of ECs. GLUT1: Glucose transporter 1; EC: Endothelial cell; AGE: Advanced glycosylation end-products; ROS: Reactive oxygen species; PARP-1: Poly polymerase 1; ADP: Adenosine diphosphate; GAPDH: Glyceraldehyde-3-phosphate dehydrogenase.