New insights into oxidative stress and inflammation during diabetes mellitus-accelerated atherosclerosis.

Published

Journal Article (Review)

Oxidative stress and inflammation interact in the development of diabetic atherosclerosis. Intracellular hyperglycemia promotes production of mitochondrial reactive oxygen species (ROS), increased formation of intracellular advanced glycation end-products, activation of protein kinase C, and increased polyol pathway flux. ROS directly increase the expression of inflammatory and adhesion factors, formation of oxidized-low density lipoprotein, and insulin resistance. They activate the ubiquitin pathway, inhibit the activation of AMP-protein kinase and adiponectin, decrease endothelial nitric oxide synthase activity, all of which accelerate atherosclerosis. Changes in the composition of the gut microbiota and changes in microRNA expression that influence the regulation of target genes that occur in diabetes interact with increased ROS and inflammation to promote atherosclerosis. This review highlights the consequences of the sustained increase of ROS production and inflammation that influence the acceleration of atherosclerosis by diabetes. The potential contributions of changes in the gut microbiota and microRNA expression are discussed.

Full Text

Duke Authors

Cited Authors

  • Yuan, T; Yang, T; Chen, H; Fu, D; Hu, Y; Wang, J; Yuan, Q; Yu, H; Xu, W; Xie, X

Published Date

  • January 2019

Published In

Volume / Issue

  • 20 /

Start / End Page

  • 247 - 260

PubMed ID

  • 30384259

Pubmed Central ID

  • 30384259

Electronic International Standard Serial Number (EISSN)

  • 2213-2317

Digital Object Identifier (DOI)

  • 10.1016/j.redox.2018.09.025

Language

  • eng

Conference Location

  • Netherlands