Dysfunctional glucose metabolism triggers oxidative stress to induce kidney injury in diabetes

Figure 1 Common complications of diabetes mellitus. Chronic hyperglycemia stimulates tissues and organs, which causes multiple problems and pathological changes including retinopathy, neuropathy, nephropathy, cardiovascular diseases, and chronic healing.

Figure 2 High glucose induces kidney cell injury and the protective effect of mizagliflozin. High glucose is absorbed into the cytosol and induces lactate dehydrogenase overexpression and thus shifts metabolism (glycolysis and fatty acid oxidation), which causes mitochondrial dysfunction. Dysfunctional mitochondria generate excessive reactive oxygen species, causing oxidative stress. Low-density lipoprotein oxidation leads to nuclear factor kappa B activation, which further triggers the expression of inflammatory factors. Oxidative stress and inflammation contribute to kidney cell injury. Mizagliflozin inhibits sodium-D-glucose cotransporter 1 and changes these processes, thus protecting cells. LDH: Lactate dehydrogenase; LDL: Low-density lipoproteins; NF-κB: Nuclear factor kappa B; ROS: reactive oxygen species; SGLT1: Sodium-D-glucose cotransporter 1.