Caifeng Fu

TL;DR: It is reported here that receptor for AGE (RAGE) is a central cell surface receptor for EN-RAGE (extracellular newly identified RAGE-binding protein) and related members of the S100/calgranulin superfamily.

TL;DR: In this article, the authors demonstrate that inhibition of RAGE-amphoterin interaction suppressed activation of p44/p42, p38 and SAP/JNK MAP kinases; molecular effector mechanisms importantly linked to tumour proliferation, invasion and expression of matrix metalloproteinases.

TL;DR: It is demonstrated here that physiologically relevant CML modifications of proteins engage cellular RAGE, thereby activating key cell signaling pathways such as NF-κB and modulating gene expression, and triggers processes intimately linked to accelerated vascular and inflammatory complications that typify disorders in which inflammation is an established component.

TL;DR: AGEs, through RAGE, may prime pro inflammatory mechanisms in endothelial cells, thereby amplifying proinflammatory mechanisms in atherogenesis and chronic inflammatory disorders.

TL;DR: CML is a major AGE in renal basement membranes in diabetic nephropathy, and its accumulation involves upregulation of RAGE on podocytes, as assessed pathologically.