Diabetic polyneuropathy (DPN) is the most common microvascular complication in diabetes mellitus (DM). The nerve fibers injury was caused by the interaction between metabolic and vascular factor. Prolonged hyperglycemia will induce several mechanisms, such as sorbitol pathway, hypoxia, oxidative stress, and increased of advanced glycation end products (AGE). Those mechanisms will trigger the production of vascular endothelial growth factor (VEGF). The production of VEGF in neovascularization was followed by the changes in microvascular structure that were marked by the enhancement of arteriol basal membrane, vein distention, arteriovenous shunting, intimal hyperplasia and hypertrophy, and endothelial fenestration. The VEGF production was a response to the hyperglycemia that was considered related to endotheliopathy and increased vascular permeability. Therefore, VEGF was acknowledged to contribute to hypoxia and acts as a potential proinflammatory substance. Nevertheless, VEGF also was considered to have a neuroprotective activity by its capability to trigger remyelination and neurogenesis. Based on this evidence, VEGF was assumed to have 2 different roles (dual effect) which are first by acting in the pathogenesis of DPN by induced hypoxia, increased vascular permeability, and caused inflammation, and second acts as a protective agent by induced nerve regeneration. This review is aimed to describe the proposed role of VEGF in the pathogenesis of DPN as well as some genetic studies regarding VEGF gene and its association with DPN.
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