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.
Keywords: Neuroinflammation, NF-kB pathway, neurodegeneration, RAGE signaling, oxidative stress.
CNS & Neurological Disorders - Drug Targets
Title:Receptor for AGEs (RAGE) as Mediator of NF-kB Pathway Activation in Neuroinflammation and Oxidative Stress
Volume: 13 Issue: 9
Author(s): Julio C. Tobon-Velasco, Elvis Cuevas and Mónica A. Torres-Ramos
Affiliation:
Keywords: Neuroinflammation, NF-kB pathway, neurodegeneration, RAGE signaling, oxidative stress.
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.
Export Options
About this article
Cite this article as:
Tobon-Velasco C. Julio, Cuevas Elvis and Torres-Ramos A. Mónica, Receptor for AGEs (RAGE) as Mediator of NF-kB Pathway Activation in Neuroinflammation and Oxidative Stress, CNS & Neurological Disorders - Drug Targets 2014; 13 (9) . https://dx.doi.org/10.2174/1871527313666140806144831
DOI https://dx.doi.org/10.2174/1871527313666140806144831 |
Print ISSN 1871-5273 |
Publisher Name Bentham Science Publisher |
Online ISSN 1996-3181 |
Call for Papers in Thematic Issues
Diagnosis and treatment of central nervous system infectious diseases
Infectious diseases of the central nervous system (CNS) can be divided into bacterial, tuberculous, viral, fungal, parasitic infections, etc. Early etiological treatment is often the most crucial means to reduce the mortality rate of patients with central nervous system infections, reduce complications and sequelae, and improve prognosis. The initial clinical ...read more
Trends and perspectives in the rational management of CNS disorders
Central nervous system (CNS) diseases enforce a significant global health burden, driving ongoing efforts to improve our understanding and effectiveness of therapy. This issue investigates current advances in the discipline, focusing on the understanding as well as therapeutic handling of various CNS diseases. The issue covers a variety of diseases, ...read more
- Author Guidelines
- Graphical Abstracts
- Fabricating and Stating False Information
- Research Misconduct
- Post Publication Discussions and Corrections
- Publishing Ethics and Rectitude
- Increase Visibility of Your Article
- Archiving Policies
- Peer Review Workflow
- Order Your Article Before Print
- Promote Your Article
- Manuscript Transfer Facility
- Editorial Policies
- Allegations from Whistleblowers
Related Articles
-
β-Lactone Derivatives and Their Anticancer Activities: A Short Review
Current Topics in Medicinal Chemistry Rational Drug Development Using Gene-Targeted Agents and Their Application in Anti-Gene Radiotherapy
Current Genomics Fibroblast Activation Protein in Remodeling Tissues
Current Molecular Medicine Alkylphospholipids are Signal Transduction Modulators with Potential for Anticancer Therapy
Anti-Cancer Agents in Medicinal Chemistry Meet Our Editorial Board Member
Current Drug Delivery Hormetic Potential of Sulforaphane (SFN) in Switching Cells’ Fate Towards Survival or Death
Mini-Reviews in Medicinal Chemistry Equinatoxin II Potentiates Temozolomide- and Etoposide-Induced Glioblastoma Cell Death
Current Topics in Medicinal Chemistry Functional Roles of the Ca2+-activated K+ Channel, KCa3.1, in Brain Tumors
Current Neuropharmacology Viral Vectors for Cancer Gene Therapy: Viral Dissemination and Tumor Targeting
Current Gene Therapy Ginkgolic Acids Confer Potential Anticancer Effects by Targeting Pro- Inflammatory and Oncogenic Signaling Molecules
Current Molecular Pharmacology Anti-Toxoplasma Activity of Natural Products: A Review
Recent Patents on Anti-Infective Drug Discovery New Molecular Targets of Anticancer Therapy – Current Status and Perspectives
Current Medicinal Chemistry Genome and Transcriptome Analysis of Neuroblastoma Advanced Diagnosis from Innovative Therapies
Current Pharmaceutical Design Transporters at CNS Barrier Sites: Obstacles or Opportunities for Drug Delivery?
Current Pharmaceutical Design The Important Roles of miR-205 in Normal Physiology, Cancers and as a Potential Therapeutic Target
Current Cancer Drug Targets B7-H3-targeted Radioimmunotherapy of Human Cancer
Current Medicinal Chemistry Using the Concept of Chous Pseudo Amino Acid Composition to Predict Enzyme Family Classes: An Approach with Support Vector Machine Based on Discrete Wavelet Transform
Protein & Peptide Letters α(N)-Heterocyclic Thiosemicarbazones: Iron Chelators that are Promising for Revival of Gallium in Cancer Chemotherapy
Anti-Cancer Agents in Medicinal Chemistry Involvement of β-arrestin-2 and Clathrin in Agonist-Mediated Internalization of the Human Cannabinoid CB2 Receptor
Current Molecular Pharmacology Molecular Mechanism of Anti-tumor Effect by Triptolide in Hematological Malignancies
Current Signal Transduction Therapy