Role of glycolysis in diabetic atherosclerosis

Figure 2 Effects of glycolysis on macrophages in hyperglycemic environment. Reactive oxygen species (ROS) induced by hyperglycemia can damage mitochondrial DNA and inhibit oxidative phosphorylation. Simultaneously, ROS can induce the expression of hypoxia-inducible factor 1α and promote glycolysis. Under the above two conditions, the ratio of M1 and M2 changes. M2 has the ability to secrete 15-lipoxygenase to promote foam cell formation and atherosclerotic protective factors such as transforming growth factor-beta, which plays an important role in maintaining plaque stability. The increase of M1 and the decrease of M2 ultimately aggravate the instability of diabetic atherosclerotic plaques. OXPHOS: Oxidative phosphorylation; AGE: Advanced glycosylation end-products; BAS: Bovine serum albumin; TGF-β: Transforming growth factor-beta; HIF-1α: Hypoxia-inducible factor 1α.