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Receptor for advanced glycation end products and its involvement in inflammatory diseases
Yaw Kuang Chuah1, Rusliza Basir, Herni Talib
1Department of Human Anatomy, Faculty of Medicine and Health Sciences, University Putra Malaysia, 43400 Serdang, Selangor, Malaysia.
Abstract:
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.
Insights
The receptor for advanced glycation end products (RAGE) is crucial in inflammation signaling. Understanding RAGE
Area of Science:
- Immunology
- Molecular Biology
- Pathology
Background:
- The receptor for advanced glycation end products (RAGE) is an immunoglobulin superfamily transmembrane receptor.
- RAGE binds diverse ligands, initiating signal transduction pathways.
- RAGE plays a role in inflammatory responses and cell activation.
Purpose of the Study:
- To review current understanding of RAGE signaling mechanisms.
- To explore RAGE's contribution to inflammation-associated diseases.
- To highlight the functional importance of RAGE in clinical settings.
Main Methods:
- Literature review of RAGE signaling pathways.
- Analysis of RAGE's role in various inflammatory conditions.
- Synthesis of evidence on molecular mechanisms.
Main Results:
- RAGE-ligand interactions activate NF-κB and increase inflammatory mediators.
- RAGE signaling is implicated in arteriosclerosis, Alzheimer's disease, arthritis, acute respiratory failure, and sepsis.
- The full clinical significance of RAGE in inflammatory diseases requires further elucidation.
Conclusions:
- RAGE is a key mediator in inflammatory signal transduction.
- Targeting RAGE pathways may offer therapeutic potential for inflammatory diseases.
- Further research is needed to fully realize RAGE's clinical importance.
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