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Advanced Glycation End Products: key player of the pathogenesis of atherosclerosis

Advanced Glycation End Products: key player of the pathogenesis of atherosclerosis Atherosclerosis is the most common type of cardiovascular disease, and it causes intima thickening, plaque development, and ultimate blockage of the artery lumen. Advanced glycation end products (AGEs) are thought to have a role in the development and progression of atherosclerosis. there is developing an enthusiasm for AGEs as a potential remedial target. AGES mainly induce arterial damage and exacerbate the development of atherosclerotic plaques by triggering cell receptor-dependent signalling. The interplay of AGEs with RAGE, a transmembrane signalling receptor present across all cells important to atherosclerosis, changes cell activity, boosts expression of genes, and increases the outflow of inflammatory compounds, resulting in arterial wall injury and plaque formation. Here in this review, function of AGEs in the genesis, progression, and instability of atherosclerosis is discussed. In endothelial and smooth muscle cells, as well as platelets, the interaction of AGEs with their transmembrane cell receptor, RAGE, triggers intracellular signalling, resulting in endothelial damage, vascular smooth muscle cell function modification, and changed platelet activity. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Glycoconjugate Journal Springer Journals

Advanced Glycation End Products: key player of the pathogenesis of atherosclerosis

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References (168)

Publisher
Springer Journals
Copyright
Copyright © The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2022
ISSN
0282-0080
eISSN
1573-4986
DOI
10.1007/s10719-022-10063-x
Publisher site
See Article on Publisher Site

Abstract

Atherosclerosis is the most common type of cardiovascular disease, and it causes intima thickening, plaque development, and ultimate blockage of the artery lumen. Advanced glycation end products (AGEs) are thought to have a role in the development and progression of atherosclerosis. there is developing an enthusiasm for AGEs as a potential remedial target. AGES mainly induce arterial damage and exacerbate the development of atherosclerotic plaques by triggering cell receptor-dependent signalling. The interplay of AGEs with RAGE, a transmembrane signalling receptor present across all cells important to atherosclerosis, changes cell activity, boosts expression of genes, and increases the outflow of inflammatory compounds, resulting in arterial wall injury and plaque formation. Here in this review, function of AGEs in the genesis, progression, and instability of atherosclerosis is discussed. In endothelial and smooth muscle cells, as well as platelets, the interaction of AGEs with their transmembrane cell receptor, RAGE, triggers intracellular signalling, resulting in endothelial damage, vascular smooth muscle cell function modification, and changed platelet activity.

Journal

Glycoconjugate JournalSpringer Journals

Published: Aug 1, 2022

Keywords: Advanced glycation end products; RAGE receptors; AGE-RAGE signalling; Atherosclerosis; Inflammation

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