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Receptor for advanced glycation end products (RAGE) and implications for the pathophysiology of heart failure

Ravichandran Ramasamy1, Ann Marie Schmidt

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

Current Heart Failure Reports
|March 30, 2012
PubMed

Insights

The receptor for advanced glycation end products (RAGE) plays a key role in heart injury and failure. Blocking RAGE shows protective effects and may offer a novel therapeutic target for heart conditions.

Area of Science:

  • Cardiovascular Biology
  • Molecular Medicine
  • Inflammation Research

Background:

  • The receptor for advanced glycation end products (RAGE) is present in various cardiac cells, including cardiomyocytes, vascular cells, and inflammatory cells.
  • RAGE and its ligands are elevated in the heart during conditions like ischemia/reperfusion injury, diabetes, and inflammation.

Purpose of the Study:

  • To investigate the role of the RAGE axis in the development and progression of heart failure.
  • To evaluate the therapeutic potential of targeting RAGE in cardiac injury models.

Main Methods:

  • Utilized murine, rat, and swine models of cardiac injury.
  • Employed pharmacological antagonism and genetic deletion of RAGE in experimental models.
  • Analyzed human studies correlating plasma levels of RAGE ligands and soluble RAGEs with heart failure severity.

Main Results:

  • RAGE and its ligands are upregulated in response to major cardiac stressors.
  • Pharmacological inhibition or genetic knockout of RAGE demonstrated significant protective effects in various cardiac injury models.
  • Elevated levels of RAGE ligands and soluble RAGEs in human plasma correlate with the severity of heart failure.

Conclusions:

  • The ligand-RAGE axis is critically involved in the pathophysiology of heart failure.
  • Therapeutic antagonism of RAGE presents a promising and unique target for treating heart failure.

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