RAGE and its ligands: A lasting memory in diabetic complications?

Shi Fang Yan, Ravichandran Ramasamy, Loredana G. Bucciarelli, Thoralf Wendt, Larisse K. Lee, Barry I. Hudson, David M. Stenr, Evanthia Lalla, Shi du Yan, Ling Ling Rong, Yoshifumi Naka, Ann Marie Schmidt

Research output: Contribution to journalArticlepeer-review

43 Scopus citations


The complications of diabetes are myriad and represent a rising cause of morbidity and mortality, particularly in the Western world. The update of the Diabetes Control and Clinical Trials Group/Epidemiology of Diabetes Interventions and Complications Research Group (DCCT/EDIC) suggested that previous strict control of hyperglycaemia was associated with reduced carotid atherosclerosis compared to conventional treatment, even after levels of glycosylated haemoglobin between the two treatment groups became indistinguishable. These intriguing findings prompt the key question, why does the blood vessel 'remember'? This review focuses on the hypothesis that the ligand/RAGE axis contributes importantly to glycaemic 'memory'. Studies in rodent models of diabetes suggest that blockade or genetic modification of RAGE suppress diabetes-associated progression of atherosclerosis, exaggerated neointimal expansion consequent to acute arterial injury, and cardiac dysfunction. We propose that therapeutic RAGE blockade will intercept maladaptive diabetes-associated memory in the vessel wall and provide cardiovascular protection in diabetes.

Original languageEnglish (US)
Pages (from-to)10-20
Number of pages11
JournalDiabetes & Vascular Disease Research
Issue number1
StatePublished - May 2004
Externally publishedYes


  • S100/calgranulins
  • amphoterin
  • glycaemic memory
  • mononuclear phagocytes
  • receptor for advanced glycation end products (RAGE)

ASJC Scopus subject areas

  • Internal Medicine
  • Endocrinology, Diabetes and Metabolism
  • Cardiology and Cardiovascular Medicine


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