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Atherosclerosis and restenosis: is there a role for RAGE?

Peter Nawroth1, Angelika Bierhaus, Mario Marrero

  • 1Dean's Office, AA152, School of Medicine, Medical College of Georgia, 1120 Fifteenth Street, Augusta, GA 30912, USA. dstern@mcg.edu

Current Diabetes Reports
|January 25, 2005
PubMed

Insights

Diabetic vascular complications are worsened by advanced glycation end product (AGE) receptor interactions. This receptor (RAGE) activation by specific ligands contributes to accelerated vascular disease in diabetes.

Area of Science:

  • Vascular biology
  • Endocrinology
  • Immunology

Background:

  • Diabetic vascular complications significantly increase morbidity and mortality.
  • Traditional risk factors inadequately explain the severity of vascular disease in diabetes.
  • Accelerated vascular disease in diabetes necessitates identifying novel pathogenic factors.

Purpose of the Study:

  • To review evidence implicating the receptor for advanced glycation end products (RAGE) in exacerbating diabetic vascular disease.
  • To explore the role of RAGE ligands in mediating cellular activation and vascular pathology in diabetes.

Main Methods:

  • Review of existing scientific literature and evidence.
  • Analysis of the role of RAGE and its ligands in the context of diabetes.
  • Examination of cellular mechanisms driven by RAGE-ligand interactions.

Main Results:

  • RAGE acts as a cofactor that exacerbates diabetic vascular disease.
  • Ligands such as nonenzymatic glycoxidation products and S100 proteins bind to RAGE.
  • This interaction drives receptor-mediated cellular activation, contributing to vascular disease.

Conclusions:

  • RAGE signaling is a key factor in the pathogenesis of accelerated diabetic vascular disease.
  • Targeting RAGE or its ligands may offer therapeutic strategies for diabetic vascular complications.

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