Diabetic polyneuropathy (DPN) is the most frequent and prevalent chronic complication of diabetes mellitus (DM). The state of\npersistent hyperglycemia leads to an increase in the production of cytosolic and mitochondrial reactive oxygen species (ROS)\nand favors deregulation of the antioxidant defenses that are capable of activating diverse metabolic pathways which trigger\nthe presence of nitro-oxidative stress (NOS) and endoplasmic reticulum stress. Hyperglycemia provokes the appearance of\nmicro- and macrovascular complications and favors oxidative damage to the macromolecules (lipids, carbohydrates, and\nproteins) with an increase in products that damage the DNA. Hyperglycemia produces mitochondrial dysfunction with\nderegulation between mitochondrial fission/fusion and regulatory factors. Mitochondrial fission appears early in diabetic\nneuropathy with the ability to facilitate mitochondrial fragmentation. Autophagy is a catabolic process induced by oxidative\nstress that involves the formation of vesicles by the lysosomes. Autophagy protects cells from diverse stress factors and\nroutine deterioration. Clarification of the mechanisms involved in the appearance of complications in DM will facilitate the\nselection of specific therapeutic options based on the mechanisms involved in the metabolic pathways affected. Nowadays, the\nantioxidant agents consumed exogenously form an adjuvant therapeutic alternative in chronic degenerative metabolic\ndiseases, such as DM.
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