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Vascular effects of advanced glycation endproducts: Clinical effects and molecular mechanisms

Authors
  • Stirban, Alin
  • Gawlowski, Thomas
  • Roden, Michael1, 2, 3, 4, 5, 6, 7
  • 1 Profil Institute for Metabolic Research GmbH
  • 2 University of Paderborn
  • 3 Institute for Clinical Diabetology
  • 4 German Diabetes Center
  • 5 Leibniz Institute for Diabetes Research at Heinrich Heine University
  • 6 Division of Endocrinology and Diabetology
  • 7 University Clinics Düsseldorf
Type
Published Article
Journal
Molecular Metabolism
Publisher
Elsevier BV
Publication Date
Jan 01, 2013
Accepted Date
Nov 18, 2013
Volume
3
Issue
2
Pages
94–108
Identifiers
DOI: 10.1016/j.molmet.2013.11.006
Source
Elsevier
Keywords
License
Unknown

Abstract

The enhanced generation and accumulation of advanced glycation endproducts (AGEs) have been linked to increased risk for macrovascular and microvascular complications associated with diabetes mellitus. AGEs result from the nonenzymatic reaction of reducing sugars with proteins, lipids, and nucleic acids, potentially altering their function by disrupting molecular conformation, promoting cross-linking, altering enzyme activity, reducing their clearance, and impairing receptor recognition. AGEs may also activate specific receptors, like the receptor for AGEs (RAGE), which is present on the surface of all cells relevant to atherosclerotic processes, triggering oxidative stress, inflammation and apoptosis. Understanding the pathogenic mechanisms of AGEs is paramount to develop strategies against diabetic and cardiovascular complications.

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