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Is the neutrophil extracellular trap-driven microvascular inflammation essential for diabetes vasculopathy?

Alexander Berezin 1, *
  1. Consultant of Therapeutic Unit, Internal Medicine Department, State Medical University for Zaporozhye, Ukraine
Correspondence to: Alexander Berezin, Consultant of Therapeutic Unit, Internal Medicine Department, State Medical University for Zaporozhye, Ukraine. Email: [email protected].
Volume & Issue: Vol. 3 No. 05 (2016) | Page No.: 618-624 |
Published: 2016-05-27

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This article is published with open access by BioMedPress. This article is distributed under the terms of the Creative Commons Attribution License (CC-BY 4.0) which permits any use, distribution, and reproduction in any medium, provided the original author(s) and the source are credited. 

Abstract

The neutrophil extracellular traps (NETs) are defined as an extensive web consisting decondensed chromatin, which is released from activated neutrophils, as well as cytotoxic proteins, histones and microbicidal proteases that cause tissue damage. NETs contribute to endothelial damage, inflammation, thrombosis, platelet aggregation, ischemia, that are essential players in the pathobiology of diabetic complications. The objective of the review is to highlight the possible role of NETosis in early diabetes-related vasculopathy beyond cardiovascular complications. Although the clinical significance of NETosis in diabetes beyond early atherosclerosis and cardiovascular complications is not still clear, there is limited data with respect to useful to use biological markers of NETosis aimed early stratification of the diabetics at risk of disease progression. Furthermore, several inductors of NETosis might be a target for novel pharmacological approaches to delay advance in diabetes and prevent diabetes-related vasculopathy.

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