Age-rage: eine Hypothese oder ein Mechanismus?

Research output: Contribution to journalReview articleContributedpeer-review


  • Berend Isermann - , University Hospital Heidelberg (Author)
  • Angelika Bierhaus - (Author)
  • Per M Humpert - (Author)
  • Gottfried Rudofsky - (Author)
  • Triantafyllos Chavakis - , Heidelberg University  (Author)
  • Robert Ritzel - (Author)
  • Thoralf Wendt - (Author)
  • Michael Morcos - (Author)
  • Christian Kasperk - (Author)
  • Andreas Hamann - (Author)
  • Peter P Nawroth - , Department of internal Medicine 3 (Author)


Acausal relation between hyperglycemia and accelerated atherosclerosis has been recently suggested. The AGE-RAGE interaction is a potential mechanism underlying the accelerated atherosclerosis. Hyperglycemia causes via nonenzymatic glycation the formation of AGEs (advanced glycation endproducts). AGEs as well as other ligands like S100/Calgranulin and Amphoterin mediate receptor-independent and -dependent (via the interaction with RAGE) effects. The ligand-RAGE-interaction results in an activation of NF-kappaB, increased expression of cytokines, chemokines, and adhesion molecules and induces oxidative stress. A relevant role of the ligand-RAGE-interaction has been demonstrated in in vivo studies, both for the accelerated atherosclerosis and increased neointima formation in diabetes mellitus. Recent data analysing atherosclerotic lesions of diabetic patients provide further evidence for the pathogenetic role of the RAGE-ligand-interaction. In addition, new experimental data established that AGEs interact with other receptors than RAGE, while RAGE interacts with a diverse group of ligands. Thus, further studies are needed for the characterization of the ligand-RAGE-interaction. These studies will provide a rationale for the development of new therapeutic approaches for accelerated atherosclerosis in diabetes mellitus.

Translated title of the contribution
a hypothesis or a mechanism?


Original languageGerman
Pages (from-to)504-9
Number of pages6
Issue number5
Publication statusPublished - Aug 2004

External IDs

Scopus 4444221879



  • Animals, Atherosclerosis/immunology, Cytokines/immunology, Glycation End Products, Advanced/immunology, Humans, Hyperglycemia/immunology, Models, Immunological, Oxidative Stress/immunology, Signal Transduction/immunology