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Receptor for Advanced Glycation End Products (RAGE) and Implications for the Pathophysiology of Heart Failure

Current Heart Failure Reports volume 9, pages 107–116 (2012)Cite this article

Abstract

The receptor for advanced glycation end products (RAGE) is expressed in the heart in cardiomyocytes, vascular cells, fibroblasts, and in infiltrating inflammatory cells. Experiments in murine, rat, and swine models of injury suggest that RAGE and the ligands of RAGE are upregulated in key injuries to the heart, including ischemia/reperfusion injury, diabetes, and inflammation. Pharmacological antagonism of RAGE or genetic deletion of the receptor in mice is strikingly protective in models of these stresses. Data emerging from human studies suggest that measurement of levels of RAGE ligands or soluble RAGEs in plasma or serum may correlate with the degree of heart failure. Taken together, the ligand-RAGE axis is implicated in heart failure and we predict that therapeutic antagonism of RAGE might be a unique target for therapeutic intervention in this disorder.

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  1. Diabetes Research Program, Division of Endocrinology, Department of Medicine, NYU School of Medicine, 550 First Avenue, Smilow 901, New York, NY, 10016, USA

    Ravichandran Ramasamy & Ann Marie Schmidt

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  1. Ravichandran Ramasamy
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  2. Ann Marie Schmidt
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Correspondence to Ann Marie Schmidt.

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Ramasamy, R., Schmidt, A.M. Receptor for Advanced Glycation End Products (RAGE) and Implications for the Pathophysiology of Heart Failure. Curr Heart Fail Rep 9, 107–116 (2012). https://doi.org/10.1007/s11897-012-0089-5

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Keywords

  • Receptor
  • Diabetes
  • RAGE
  • Myocarditis
  • Inflammation
  • Ischemia
  • Reperfusion
  • Glycation
  • S100/calgranulin
  • HMGB1
  • Soluble RAGE
  • Heart failure
  • Cardiomyocyte
  • Fibroblast
  • Endothelium
  • Pathophysiology