RAGE: therapeutic target and biomarker of the inflammatory response-the evidence mounts

被引：225

作者：

Ramasamy, Ravichandran ^{[1
]}

Yan, Shi Fang ^{[1
]}

Schmidt, Ann Marie ^{[1
]}

机构：

[1] Columbia Univ, Div Surg Sci, Dept Surg, Coll Phys & Surg, New York, NY 10032 USA

来源：

JOURNAL OF LEUKOCYTE BIOLOGY | 2009年 / 86卷 / 03期

关键词：

glycation; oxidation; S100; HMGB1; inflammation; GLYCATION END-PRODUCTS; CELL-SURFACE RECEPTOR; NF-KAPPA-B; SOLUBLE RECEPTOR; NEURITE OUTGROWTH; DIABETIC-NEPHROPATHY; SIGNALING PATHWAYS; CYTOPLASMIC DOMAIN; ENDOTHELIAL-CELLS; BINDING-PROTEINS;

D O I：

10.1189/jlb.0409230

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

The RAGE binds multiple ligand families linked to hyperglycemia, aging, inflammation, neurodegeneration, and cancer. Activation of RAGE by its ligands stimulates diverse signaling cascades. The recent observation that the cytoplasmic domain of RAGE interacts with diaphanous or mDia-1 links RAGE signal transduction to cellular migration and activation of the Rho GTPases, cdc42 and rac-1. Pharmacological blockade of RAGE or genetic deletion of RAGE imparts significant protection in murine models of diabetes, inflammatory conditions, Alzheimer's disease, and tumors. Intriguingly, soluble forms of RAGE, including the splice variant-derived esRAGE, circulate in human plasma. Studies in human subjects suggest that sRAGE levels may be modulated by the diseases impacted by RAGE and its ligands. Thus, in addition to being a potential therapeutic target in chronic disease, monitoring of plasma sRAGE levels may provide a novel biomarker platform for tracking chronic inflammatory diseases, their severity, and response to therapeutic intervention. J. Leukoc. Biol. 86: 505-512; 2009.

引用

页码：505 / 512

页数：8

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