Receptor for AGEs (RAGE) as mediator of NF-kB pathway activation in neuroinflammation and oxidative stress

Julio C. Tobón-Velasco, Elvis Cuevas, MóNica A. Torres-Ramos

Research output: Contribution to journalArticlepeer-review

166 Scopus citations

Abstract

Recently, it has been proposed that the receptor for advanced glycation end-products (RAGE) plays a crucial role in damaging cellular processes, such as neuroinflammation, neurodegeneration, excitotoxicity and oxidative stress. RAGE is a multiligand receptor belonging to the immunoglobulin superfamily of cell surface molecules acting as a counter-receptor for diverse molecules. Engagement of RAGE converts a brief pulse of cellular activation into sustained cellular dysfunction and tissue damage. Indeed, the involvement of RAGE in physiopathological processes has been demonstrated for several neurodegenerative diseases. It is the full-length form of RAGE the one constituting the cellular receptor which is able to activate intracellular signals. After the binding of ligands to RAGE, oxidative stress is increased; then, over-expression of RAGE produces vicious cycles that perpetuate oxidative stress and contribute to neuroinflammation by nuclear factor-kB (NF-kB) up-regulation. The NF-kB activation promotes the expression of proinflammatory cytokines, including RAGE expression, to induce a prolonged activation and promotion of signaling mechanisms for cell damage. Because inflammatory and oxidative events have been demonstrated to concertedly interact during neurodegenerative events, this review is aimed to discuss the role of RAGE as mediator of an interaction between inflammation and oxidative stress through NF-kB signaling pathway.

Original languageEnglish (US)
Pages (from-to)1615-1626
Number of pages12
JournalCNS and Neurological Disorders - Drug Targets
Volume13
Issue number9
DOIs
StatePublished - Jan 1 2014
Externally publishedYes

Keywords

  • Neurodegeneration
  • Neuroinflammation
  • NF-kB pathway
  • Oxidative stress
  • RAGE signaling

ASJC Scopus subject areas

  • Neuroscience(all)
  • Pharmacology

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