scholarly journals Advanced glycation end-products disrupt brain microvascular endothelial cell barrier: The role of mitochondria and oxidative stress

2021 ◽  
Vol 133 ◽  
pp. 104098
Author(s):  
Anthony Dobi ◽  
Sarah Rosanaly ◽  
Anne Devin ◽  
Pascal Baret ◽  
Olivier Meilhac ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cell ◽  
Advanced Glycation End Products ◽  
Microvascular Endothelial Cell ◽  
Brain Microvascular Endothelial Cell ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
End Products ◽  
And Oxidative Stress

Role of Advanced Glycation End Products (AGEs) and Oxidative Stress in Diabetic Retinopathy

2008 ◽  
Vol 14 (10) ◽  
pp. 962-968 ◽  
Author(s):  
Sho-ichi Yamagishi ◽  
Seiji Ueda ◽  
Takanori Matsui ◽  
Kazuo Nakamura ◽  
Seiya Okuda
Keyword(s):  
Oxidative Stress ◽  
Diabetic Retinopathy ◽  
Advanced Glycation End Products ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
End Products ◽  
And Oxidative Stress

scholarly journals Advanced Glycation End Products and Oxidative Stress in a Hyperglycaemic Environment

2021 ◽  
Author(s):  
Akio Nakamura ◽  
Ritsuko Kawahrada
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Advanced Glycation End Products ◽  
Reactive Oxygen ◽  
Protein Glycation ◽  
Oxygen Species ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
End Products ◽  
And Oxidative Stress

Protein glycation is the random, nonenzymatic reaction of sugar and protein induced by diabetes and ageing; this process is quite different from glycosylation mediated by the enzymatic reactions catalysed by glycosyltransferases. Schiff bases form advanced glycation end products (AGEs) via intermediates, such as Amadori compounds. Although these AGEs form various molecular species, only a few of their structures have been determined. AGEs bind to different AGE receptors on the cell membrane and transmit signals to the cell. Signal transduction via the receptor of AGEs produces reactive oxygen species in cells, and oxidative stress is responsible for the onset of diabetic complications. This chapter introduces the molecular mechanisms of disease onset due to oxidative stress, including reactive oxygen species, caused by AGEs generated by protein glycation in a hyperglycaemic environment.

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