Journal
REDOX BIOLOGY
Volume 20, Issue -, Pages 247-260Publisher
ELSEVIER
DOI: 10.1016/j.redox.2018.09.025
Keywords
Atherosclerosis; Diabetes mellitus; Reactive oxygen species; Gut microbiota; MicroRNA
Categories
Funding
- National Undergraduate Innovation and Entrepreneurship Training Program [201710632002]
- Luzhou City Bureau of Science and Technology [2016LZXNYD-J26]
- Scientific Research Fund of SiChuan Provincial Education Department [17ZA0426, 17ZA0433]
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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.
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