| An update on advanced glycation endproducts and atherosclerosis. | |
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MedLine Citation:
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PMID: 22488968 Owner: NLM Status: Publisher |
Abstract/OtherAbstract:
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Advanced glycation endproducts (AGEs) are a group of modified molecular species formed by nonenzymatic reactions between the aldehydic group of reducing sugars with proteins, lipids, or nucleic acids. Formation and accumulation of AGEs are related to the aging process and are accelerated in diabetes. AGEs are generated in hyperglycemia, but their production also occurs in settings characterized by oxidative stress and inflammation. These species promote vascular damage and acceleration of atherosclerotic plaque progression mainly through two mechanisms: directly, altering the functional properties of vessel wall extracellular matrix molecules, or indirectly, through activation of cell receptor-dependent signaling. Interaction between AGEs and the key receptor for AGEs (RAGE), a transmembrane signaling receptor which is present in all cells relevant to atherosclerosis, alters cellular function, promotes gene expression, and enhances the release of proinflammatory molecules. The importance of the AGE-RAGE interaction and downstream pathways, leading to vessel wall injury and plaque development, has been amply established in animal studies. Moreover, the deleterious link of AGEs with diabetic vascular complications has been suggested in many human studies. Blocking the vicious cycle of AGE-RAGE axis signaling may be essential in controlling and preventing cardiovascular complications. In this article, we review the pathogenetic role of AGEs in the development, progression and instability of atherosclerosis, and the potential targets of this biological system for the prevention and treatment of cardiovascular disease. © 2012 International Union of Biochemistry and Molecular Biology, Inc. |
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Authors:
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Serena Del Turco; Giuseppina Basta |
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Publication Detail:
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Type: JOURNAL ARTICLE Date: 2012-4-10 |
Journal Detail:
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Title: BioFactors (Oxford, England) Volume: - ISSN: 1872-8081 ISO Abbreviation: - Publication Date: 2012 Apr |
Date Detail:
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Created Date: 2012-4-10 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 8807441 Medline TA: Biofactors Country: - |
Other Details:
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Languages: ENG Pagination: - Citation Subset: - |
Copyright Information:
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Copyright © 2012 International Union of Biochemistry and Molecular Biology, Inc. |
Affiliation:
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Institute of Clinical Physiology, National Research Council (CNR), Pisa, Italy. |
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