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• W1995560198 endingPage "247" @default.
• W1995560198 startingPage "193" @default.
• W1995560198 abstract "Neuroinflammation is a CNS reaction to injury in which some severe pathologies, regardless of their origin, converge. The phenomenon emphasizes crosstalk between neurons and glia and reveals a complex interaction with oxidizing agents through redox sensors localized in enzymes, receptors, and transcription factors. When oxidizing pressures cause reversible molecular changes, such as minimal or transitory proinflammatory cytokine overproduction, redox couples provide a means of translating the presence of reactive oxygen or nitrogen species into useful signals in the cell. Additionally, thiol-based redox sensors convey information about localized changes in redox potential induced by physiologic or pathologic situations. They are susceptible to oxidative changes and become key events during neuroinflammation, altering the course of a signaling response or the behavior of specific transcription factors. When oxidative stress augments the pressure on the intracellular environment, the effective reduction potential of redox pairs diminishes, and cell signaling shifts toward proinflammatory and proapoptotic signals, creating a vicious cycle between oxidative stress and neuroinflammation. In addition, electrophilic compounds derived from the oxidative cascade react with key protein thiols and interfere with redox signaling. This article reviews the relevant functional aspects of redox control during the neuroinflammatory process. Antioxid. Redox Signal. 13, 193–247. Introduction Definitions and scope Innate Immune Response in the Central Nervous System Neuroinflammation is a team effort Microglia respond to their environment Astrocytes and neurons as microglia modulators Neuroinflammation and Redox Homeostasis Endogenous danger signals in neuroinflammation and their relation to redox variations Extracellular ATP: immunomodulatory, NOX/H2O2 inducer, and possibly, a denitrosylating agent: its role in neurodegenerative pathologies HMGB1, a redox-regulated danger signal The extracellular S100B activities rely on the oxidation of the protein cysteine residues The influence of redox regulation in the crosstalk between innate and adaptive immune systems through Hsps Other endogenous signs of damage Thiol-based redox sensors Redox sensors in neuroinflammation Redox status and proinflammatory mediators Dual role of TNF Oxidative/Nitrosative Stress Steady-state levels of reactive species S-nitrosylation in neurodegenerative disorders Role of GSH Depletion and Its Replenishment Dynamic Redox Control in Neuroinflammatory Processes: Glutathionylation/Deglutathionylation Redox Control of Enzymes Involved in Neuroinflammation NADPH-oxidase is controlled by redox variations Microglial overactivated NOX in neuroinflammatory diseases An oxidizable antioxidant, SOD Main Redox-Related Pathways in Neuroinflammation The central innate immune sensors: Toll-like receptors A redox-regulated pathway and a target to reduce neurodegeneration and neuroinflammation: Nrf2 Electrophiles attack Keap1 and provide neuroprotection The redox-regulated hypoxia-inducible transcription factor-1: its role beyond ischemia HIF-1α a very active protagonist in neuroinflammation Redox-regulated NMDAR Fats and Alternative Mechanisms of Redox Regulation Oxidation of N-6 PUFAs ApoE in detoxifying HNE, an example of functional aspects of redox regulation 15Δ-PGJ2, a controversy around electrophilic compounds The immunoregulatory and redox-regulated PPARs Redox-Regulated transcription factors NF-κB a pluripotential key regulator of neuroinflammation Redox regulation of NF-κB Redox-regulated pathways involved in NF-κB activation DNA-binding properties of AP-1 depend on the redox state of its cysteine residues Reactive cysteines contribute to a negative regulation for p53 Phosphorylation and Redox Considerations Concurrent pathways Redox Changes Linked to the Pathophysiology of Neuroinflammatory/Neurodegenerative Diseases: A Tentative Classification Particular disease-related alterations Redox-regulatable processes common to neurodegenerative diseases Neurofilament-related alterations Protein aggregate–related alterations Mitochondrial dysfunction and energy failure–related alterations General stress-related pathophysiologic mechanisms Processes related to the neuroinflammatory response, including signaling pathways Antiapoptotic or proapoptotic responses Related to the antioxidant response Related to synaptic transmission and excitotoxic stress Common alterations related to lipids Concluding Remarks Major progress Problems Prospects in the field" @default.
• W1995560198 created "2016-06-24" @default.
• W1995560198 creator A5029032735 @default.
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• W1995560198 creator A5083210149 @default.
• W1995560198 creator A5088424354 @default.
• W1995560198 date "2010-07-15" @default.
• W1995560198 modified "2023-10-18" @default.
• W1995560198 title "Functional Aspects of Redox Control During Neuroinflammation" @default.
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