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
Techniques of Drug Repurposing: Delivering a new life to Herbs & Drugs
Of late, with the adaptation of innovative approaches and integration of advancements made towards medical sciences as well as the availability of a wide range of tools; several therapeutic challenges are being translated into viable clinical solutions, with a high degree of efficacy, safety, and selectivity. With a better understanding ...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
-
Translating Mismatch Repair Mechanism into Cancer Care
Current Drug Targets Tumor Dormancy and the Angiogenic Switch: Possible Implications of Bone Marrow- Derived Cells
Current Pharmaceutical Design Gene Transfer to the Central Nervous System: Current State of the Art of the Viral Vectors
Current Genomics One-Step Synthesis of 1H-1,2,3-Triazol-1-Ylmethyl-2,3-Dihydronaphtho[1,2-b]furan- 4,5-Diones
Current Organic Synthesis Apoptosis-Inducing Effects of Amaryllidaceae Alkaloids
Current Medicinal Chemistry Blockade of Ser16-Hsp20 Phosphorylation Attenuates Neuroprotection Dependent Upon Bcl-2 and Bax
Current Neurovascular Research Recent Developments in Taxane Drug Delivery
Current Drug Delivery Aneurysm of the Communicating Vein Between the Left Renal Vein and Left Ascending Lumbar Vein Mimicking Retroperitoneal Lymphadenopathy: A Case Report
Current Medical Imaging Discussion on the Structural Modification and Anti-tumor Activity of Flavonoids
Current Topics in Medicinal Chemistry Cancer Stem Cells in Pediatric Brain Tumors
Current Stem Cell Research & Therapy Recent Advancements in Nanodiamond Mediated Brain Targeted Drug Delivery and Bioimaging of Brain Ailments: A Holistic Review
Pharmaceutical Nanotechnology Development of Selective High Affinity Antagonists, Agonists, and Radioligands for the P2Y1 Receptor
Combinatorial Chemistry & High Throughput Screening Cellular Based Cancer Vaccines: Type 1 Polarization of Dendritic Cells
Current Medicinal Chemistry Sirtuin Inhibitors: An Overview from Medicinal Chemistry Perspective
Anti-Cancer Agents in Medicinal Chemistry Lipid-Based Drug Delivery Systems for Cancer Treatment
Current Drug Targets The Influence of Ionizing Radiation on Exosome Composition, Secretion and Intercellular Communication
Protein & Peptide Letters ErbB Targeted Drugs and Angiogenesis
Current Vascular Pharmacology Dysfunction of Mitochondrial ATP Production As a Target for Personalized Cancer Therapy
Current Pharmacogenomics and Personalized Medicine Lipoxygenase (LOX) Pathway: A Promising Target to Combat Cancer
Current Pharmaceutical Design Central Nervous System Vasculitis: Still More Questions than Answers
Current Neuropharmacology