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RAGE: therapeutic target and biomarker of the inflammatory response--the evidence mounts.
- Source :
-
Journal of leukocyte biology [J Leukoc Biol] 2009 Sep; Vol. 86 (3), pp. 505-12. Date of Electronic Publication: 2009 May 28. - Publication Year :
- 2009
-
Abstract
- 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.
- Subjects :
- Biomarkers blood
Glycation End Products, Advanced genetics
Humans
Inflammation genetics
Ligands
Models, Immunological
Polymorphism, Single Nucleotide
Protein Binding genetics
Protein Structure, Tertiary
Receptor for Advanced Glycation End Products
Receptors, Immunologic blood
Receptors, Immunologic chemistry
Receptors, Immunologic genetics
Signal Transduction
Solubility
Glycation End Products, Advanced metabolism
Inflammation metabolism
Receptors, Immunologic metabolism
Subjects
Details
- Language :
- English
- ISSN :
- 1938-3673
- Volume :
- 86
- Issue :
- 3
- Database :
- MEDLINE
- Journal :
- Journal of leukocyte biology
- Publication Type :
- Academic Journal
- Accession number :
- 19477910
- Full Text :
- https://doi.org/10.1189/jlb.0409230