Review Article

Diabetic Neuropathy and Oxidative Stress: Therapeutic Perspectives

Figure 2

Mechanisms of diabetic neuropathy. The AGE and polyol pathways directly alter the redox capacity of the cell either through depletion of necessary components of glutathione recycling or by direct formation of ROS. The hexosamine, PKC, and PARP pathways indicate damage through expression of inflammation proteins. Dyslipidaemia with high incidence in T2D also linked to DN, and several underlying mechanisms have been identified. AGEs: advanced glycation end products; RAGEs: receptor for advanced glycation end products; NF-κB: nuclear factor kappa B; AD: aldose reductase; SDH: sorbitol dehydrogenase; GSH: glutathione; GSSG: oxidized glutathione; F-6-P: fructose-6 phosphate; UDPGlcNAc: uridine diphosphate-N-acetylglucosamine; PAI-1: plasminogen activator inhibitor-1; TGF-β1: transforming growth factor-β1; DAG: diaceylglycerol; PKC: protein kinase C; ROS: reactive oxygen species; RNS: reactive nitrogen species; PARP: poly ADP-ribose polymerase; Mt: mitochondria; MMPs: mitochondrial membrane potentials; Cyc: cytochrome c; NO: nitric oxide; LDL: low-density lipoprotein; LOX1: oxidised LDL receptor 1; TLR4: toll-like receptor 4; FFA: free fatty acids; TG: triglycerides; HDL: high-density lipoprotein; CyK: cytokine.
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