Fig. 1.

RAGE ligands-RAGE axis contributes to cardiac dysfunction and failure. The ligand-RAGE axis acts via both cell autonomous and cell non-autonomous mechanisms to enhance stress in the myocardium consequent to I/R, diabetes, or inflammation. We propose that the balance of RAGE action in these settings increases damage and blocks adaptive regeneration. Blockade of ligand-RAGE may be a targeted therapeutic strategy for strategies to salvage stressed myocardium. I/R ischemia/reperfusion; AGEs advanced glycation end products; HMGB1 high-mobility group protein B1; RAGE receptor for advanced glycation end products