Receptor for Advanced Glycation End Products and Its Involvement in Inflammatory Diseases

The receptor for advanced glycation end products (RAGE) is a transmembrane receptor of the immunoglobulin superfamily, capable of binding a broad repertoire of ligands. RAGE-ligands interaction induces a series of signal transduction cascades and lead to the activation of transcription factor NF-κB...

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Main Authors: Chuah, Yaw Kuang, Basir, Rusliza, Talib, Herni, Tie, Tung Hing, Nordin, Norshariza
Format: Online
Language:English
Published: Hindawi Publishing Corporation 2013
Online Access:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3786507/
id pubmed-3786507
recordtype oai_dc
spelling pubmed-37865072013-10-07 Receptor for Advanced Glycation End Products and Its Involvement in Inflammatory Diseases Chuah, Yaw Kuang Basir, Rusliza Talib, Herni Tie, Tung Hing Nordin, Norshariza Review Article The receptor for advanced glycation end products (RAGE) is a transmembrane receptor of the immunoglobulin superfamily, capable of binding a broad repertoire of ligands. RAGE-ligands interaction induces a series of signal transduction cascades and lead to the activation of transcription factor NF-κB as well as increased expression of cytokines, chemokines, and adhesion molecules. These effects endow RAGE with the role in the signal transduction from pathogen substrates to cell activation during the onset and perpetuation of inflammation. RAGE signaling and downstream pathways have been implicated in a wide spectrum of inflammatory-related pathologic conditions such as arteriosclerosis, Alzheimer's disease, arthritis, acute respiratory failure, and sepsis. Despite the significant progress in other RAGE studies, the functional importance of the receptor in clinical situations and inflammatory diseases still remains to be fully realized. In this review, we will summarize current understandings and lines of evidence on the molecular mechanisms through which RAGE signaling contributes to the pathogenesis of the aforementioned inflammation-associated conditions. Hindawi Publishing Corporation 2013 2013-09-11 /pmc/articles/PMC3786507/ /pubmed/24102034 http://dx.doi.org/10.1155/2013/403460 Text en Copyright © 2013 Yaw Kuang Chuah et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
repository_type Open Access Journal
institution_category Foreign Institution
institution US National Center for Biotechnology Information
building NCBI PubMed
collection Online Access
language English
format Online
author Chuah, Yaw Kuang
Basir, Rusliza
Talib, Herni
Tie, Tung Hing
Nordin, Norshariza
spellingShingle Chuah, Yaw Kuang
Basir, Rusliza
Talib, Herni
Tie, Tung Hing
Nordin, Norshariza
Receptor for Advanced Glycation End Products and Its Involvement in Inflammatory Diseases
author_facet Chuah, Yaw Kuang
Basir, Rusliza
Talib, Herni
Tie, Tung Hing
Nordin, Norshariza
author_sort Chuah, Yaw Kuang
title Receptor for Advanced Glycation End Products and Its Involvement in Inflammatory Diseases
title_short Receptor for Advanced Glycation End Products and Its Involvement in Inflammatory Diseases
title_full Receptor for Advanced Glycation End Products and Its Involvement in Inflammatory Diseases
title_fullStr Receptor for Advanced Glycation End Products and Its Involvement in Inflammatory Diseases
title_full_unstemmed Receptor for Advanced Glycation End Products and Its Involvement in Inflammatory Diseases
title_sort receptor for advanced glycation end products and its involvement in inflammatory diseases
description The receptor for advanced glycation end products (RAGE) is a transmembrane receptor of the immunoglobulin superfamily, capable of binding a broad repertoire of ligands. RAGE-ligands interaction induces a series of signal transduction cascades and lead to the activation of transcription factor NF-κB as well as increased expression of cytokines, chemokines, and adhesion molecules. These effects endow RAGE with the role in the signal transduction from pathogen substrates to cell activation during the onset and perpetuation of inflammation. RAGE signaling and downstream pathways have been implicated in a wide spectrum of inflammatory-related pathologic conditions such as arteriosclerosis, Alzheimer's disease, arthritis, acute respiratory failure, and sepsis. Despite the significant progress in other RAGE studies, the functional importance of the receptor in clinical situations and inflammatory diseases still remains to be fully realized. In this review, we will summarize current understandings and lines of evidence on the molecular mechanisms through which RAGE signaling contributes to the pathogenesis of the aforementioned inflammation-associated conditions.
publisher Hindawi Publishing Corporation
publishDate 2013
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3786507/
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