A Soluble Receptor for Advanced Glycation End‐Products Attenuates Myocardial Ischemia/Reperfusion Injury via Enhancing Glucose Metabolism

, and adenosine triphosphate levels in cardiomyocytes during OGD/R. sRAGE activated the AMP-activated protein kinase (AMPK)/Akt substrate of 160 kDa (AS160) signaling pathway, and the application of AMPK inhibitor or AS160 mutant abolished the effect of sRAGE on facilitating plasma membrane GLUT4 localization and glucose metabolism. Moreover, the AMPK inhibitor or silenced GLUT4 depleted the anti-apoptotic effect of sRAGE during OGD/R in cardiomyocytes. Therefore, it was suggested that sRAGE inhibited I/R-induced apoptosis via enhancing the GLUT4 translocation to the plasma membrane and glucose metabolism through the AMPK/AS160 signaling pathway.