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Published on: September 15, 2017

RAGE in inflammation: a new therapeutic target?

Angelika Bierhaus1, David M Stern, Peter P Nawroth

  • 1Department of Medicine I, University of Heidelberg, INF 410, 69120 Heidelberg, Germany.

Current Opinion in Investigational Drugs (London, England : 2000)
|November 23, 2006
PubMed

Insights

Certain proteins and peptides trigger inflammation by disrupting cellular function and immune tolerance. Targeting the receptor of advanced glycation end products (RAGE) can suppress inflammation and reduce tissue damage in inflammatory disorders.

Area of Science:

  • Immunology
  • Cell Biology
  • Molecular Medicine

Background:

  • High-molecular group box 1-protein, S100/calgranulins, advanced glycation end products (AGEs), amyloid-beta peptides, and beta-sheet fibrils are implicated in inflammatory conditions.
  • These molecules promote cellular dysfunction and impair immune tolerance.
  • The receptor of AGE (RAGE) is a key pattern recognition receptor involved in these processes.

Purpose of the Study:

  • To investigate the role of RAGE in inflammatory conditions.
  • To explore RAGE as a potential therapeutic target for inflammation.

Main Methods:

  • The study focuses on the molecular interactions and signaling pathways involving RAGE and its ligands.
  • Experimental models of inflammatory disorders were used to assess the effects of RAGE deletion and RAGE-ligand interaction interruption.

Main Results:

  • RAGE acts as an endothelial adhesion receptor, promoting leukocyte recruitment and extravasation.
  • RAGE engagement leads to sustained cellular dysfunction via nuclear factor-kappaB activation.
  • Deletion of RAGE and interruption of RAGE-ligand interactions suppressed inflammation and reduced tissue damage in experimental models.

Conclusions:

  • RAGE plays a critical role in mediating inflammation and cellular dysfunction.
  • Targeting RAGE and its ligand interactions presents a promising therapeutic strategy for inflammatory disorders.

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