The role of vascular endothelial growth factor in diabetic polyneuropathy

10/15/2019 12:00:00 AM

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Authors:Jimmy Barus, Ismail Setyopranoto, Ahmad Hamim Sadewa, Samekto Wibowo

Publication date: July 26, 2018

International Journal of Medical Reviews and Case Rerports

Volume:  -

Link: https://www.ejmanager.com/mnstemps/172/172-1530806385.pdf?t=1533104224

 

 

ABSTRACT Diabetic polyneuropathy (DPN) is the most common  microvascular complication in diabetes  mellitus  (DM). The nerve  fibres 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 neovascularisation was  followed by the  changes in microvascular structure that  were marked by the enhancement of arterial 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.

 

KEYWORDS VEGF, vascular endothelial growth factor, diabetic polyneuropathy, DPN