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
-
Emerging Adenoviral Vectors for Stable Correction of Genetic Disorders
Current Gene Therapy Small Molecules for Immunomodulation in Cancer: A Review
Anti-Cancer Agents in Medicinal Chemistry Targeting the Phosphatidylinositol 3-Kinase/AKT Pathway for the Treatment of Multiple Myeloma
Current Medicinal Chemistry Diagnostic and Therapeutic Uses of Nanomaterials in the Brain
Current Medicinal Chemistry Metabolic and Functional Brain Mapping, Connectivity and Plasticity Applied to the Surgery of Cerebral Tumors
Current Medical Imaging Recent Advances of Natural and Synthetic β-Carbolines as Anticancer Agents
Anti-Cancer Agents in Medicinal Chemistry Crude Venom from Nematocysts of the Jellyfish Pelagia noctiluca as a Tool to Study Cell Physiology
Central Nervous System Agents in Medicinal Chemistry Identification of Novel Drug Targets for Angiostatic Cancer Therapy; It Takes Two to Tango
Current Pharmaceutical Design Inhibitors of Chronically Active Ras: Potential for Treatment of Human Malignancies
Recent Patents on Anti-Cancer Drug Discovery Peptide Prodrugs for the Treatment of CNS Disorders: A Perspective for New Drugs
Current Medicinal Chemistry Stem Cells: In Sickness and in Health
Current Stem Cell Research & Therapy Salen Mn Complexes Mitigate Radiation Injury in Normal Tissues
Anti-Cancer Agents in Medicinal Chemistry Cyclodextrins and their Derivatives as Carrier Molecules in Drug and Gene Delivery Systems
Current Organic Chemistry Glutathione Peroxidase Activity of Ebselen and its Analogues: Some Insights into the Complex Chemical Mechanisms Underlying the Antioxidant Activity
Current Chemical Biology Recent Advances in Optical Cancer Imaging of EGF Receptors
Current Medicinal Chemistry The Recent Medicinal Chemistry Development of Jak2 Tyrosine Kinase Small Molecule Inhibitors
Current Medicinal Chemistry Evaluating the Diagnostic and Chemotherapeutic Potential of Vancomycin- Derived Imaging Conjugates
Medicinal Chemistry Microglial Activation and its Implications in the Brain Diseases
Current Medicinal Chemistry Sublethal Total Body Irradiation Leads to Early Cerebellar Damage and Oxidative Stress
Current Neurovascular Research Glycoconjugates: Roles in Neural Diseases Caused by Exogenous Pathogens
CNS & Neurological Disorders - Drug Targets