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

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 a...

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Vydáno v:Molecular metabolism (Germany) Ročník 3; číslo 2; s. 94 - 108
Hlavní autoři: Stirban, Alin, Gawlowski, Thomas, Roden, Michael
Médium: Journal Article
Jazyk:angličtina
Vydáno: Germany Elsevier GmbH 01.04.2014
Elsevier
Témata:
Advanced glycation endproducts
Endocrinology & Metabolism
Endothelium
Review
Vascular
Advanced glycation endproducts
Vascular
Endothelium
ISSN:2212-8778, 2212-8778
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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.
AbstractList 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.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.
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.
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.
Author Stirban, Alin
Roden, Michael
Gawlowski, Thomas
AuthorAffiliation 4 Division of Endocrinology and Diabetology, University Clinics Düsseldorf, 40225 Düsseldorf, Germany
3 Institute for Clinical Diabetology, German Diabetes Center, Leibniz Institute for Diabetes Research at Heinrich Heine University, 40225 Düsseldorf, Germany
1 Profil Institut für Stoffwechselforschung GmbH, Hellersbergstrasse 9, 41460 Neuss, Germany
2 University of Paderborn, Warburger Str. 100, 33098 Paderborn, Germany
AuthorAffiliation_xml – name: 1 Profil Institut für Stoffwechselforschung GmbH, Hellersbergstrasse 9, 41460 Neuss, Germany
– name: 4 Division of Endocrinology and Diabetology, University Clinics Düsseldorf, 40225 Düsseldorf, Germany
– name: 3 Institute for Clinical Diabetology, German Diabetes Center, Leibniz Institute for Diabetes Research at Heinrich Heine University, 40225 Düsseldorf, Germany
– name: 2 University of Paderborn, Warburger Str. 100, 33098 Paderborn, Germany
Author_xml – sequence: 1
  givenname: Alin
  surname: Stirban
  fullname: Stirban, Alin
  email: alin.stirban@profil.com
  organization: Profil Institut für Stoffwechselforschung GmbH, Hellersbergstrasse 9, 41460 Neuss, Germany
– sequence: 2
  givenname: Thomas
  surname: Gawlowski
  fullname: Gawlowski, Thomas
  email: thgawlowski@gmail.com
  organization: University of Paderborn, Warburger Str. 100, 33098 Paderborn, Germany
– sequence: 3
  givenname: Michael
  surname: Roden
  fullname: Roden, Michael
  email: Michael.Roden@DDZ.uni-duesseldorf.de
  organization: Institute for Clinical Diabetology, German Diabetes Center, Leibniz Institute for Diabetes Research at Heinrich Heine University, 40225 Düsseldorf, Germany
BackLink https://www.ncbi.nlm.nih.gov/pubmed/24634815$$D View this record in MEDLINE/PubMed
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Snippet The enhanced generation and accumulation of advanced glycation endproducts (AGEs) have been linked to increased risk for macrovascular and microvascular...
Abstract The enhanced generation and accumulation of advanced glycation endproducts (AGEs) have been linked to increased risk for macrovascular and...
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SubjectTerms Advanced glycation endproducts
Endocrinology & Metabolism
Endothelium
Review
Vascular
Title Vascular effects of advanced glycation endproducts: Clinical effects and molecular mechanisms
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