Ferroptosis and central nervous system demyelinating diseases

Ferroptosis is a newly discovered programmed cell death caused by intracellular iron excess and glutathione (GSH) system imbalance, resulting in fatal lipid peroxidation. It is different from necrosis, apoptosis, autophagy, and other forms of cell death. Accumulating evidences suggest that brain iro...

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Published inJournal of neurochemistry Vol. 165; no. 6; pp. 759 - 771
Main Authors Qin, Danqing, Li, Dong, Wang, Chunjuan, Guo, Shougang
Format Journal Article
LanguageEnglish
Published England Blackwell Publishing Ltd 01.06.2023
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Abstract Ferroptosis is a newly discovered programmed cell death caused by intracellular iron excess and glutathione (GSH) system imbalance, resulting in fatal lipid peroxidation. It is different from necrosis, apoptosis, autophagy, and other forms of cell death. Accumulating evidences suggest that brain iron overload is involved in the pathogenesis of demyelinating diseases of the central nervous system (CNS), such as multiple sclerosis (MS), neuromyelitis optica (NMO), and acute disseminated encephalomyelitis (ADEM). The study of ferroptosis may provide a new understanding of demyelinating diseases and provide a novel therapeutic target for clinical treatment. Herein, we reviewed recent discoveries on mechanisms of ferroptosis, the effects of metabolic pathways on ferroptosis, and its involvement in CNS demyelinating diseases. Ferroptosis is the result of multiple biological pathways acting together as a newly discovered cell death program. The major metabolic pathways associated with ferroptosis susceptibility include iron metabolism, lipid metabolism, and amino acid metabolism. Ferroptosis plays a key role in the pathophysiology of central nervous system (CNS) demyelinating diseases. Blocking the process of iron death can reduce myelin damage and alleviate the neurological dysfunction caused by demyelinating diseases such as multiple sclerosis, neuromyelitis optica, and acute disseminated encephalomyelitis.
AbstractList Ferroptosis is a newly discovered programmed cell death caused by intracellular iron excess and glutathione (GSH) system imbalance, resulting in fatal lipid peroxidation. It is different from necrosis, apoptosis, autophagy, and other forms of cell death. Accumulating evidences suggest that brain iron overload is involved in the pathogenesis of demyelinating diseases of the central nervous system (CNS), such as multiple sclerosis (MS), neuromyelitis optica (NMO), and acute disseminated encephalomyelitis (ADEM). The study of ferroptosis may provide a new understanding of demyelinating diseases and provide a novel therapeutic target for clinical treatment. Herein, we reviewed recent discoveries on mechanisms of ferroptosis, the effects of metabolic pathways on ferroptosis, and its involvement in CNS demyelinating diseases.
Ferroptosis is a newly discovered programmed cell death caused by intracellular iron excess and glutathione (GSH) system imbalance, resulting in fatal lipid peroxidation. It is different from necrosis, apoptosis, autophagy, and other forms of cell death. Accumulating evidences suggest that brain iron overload is involved in the pathogenesis of demyelinating diseases of the central nervous system (CNS), such as multiple sclerosis (MS), neuromyelitis optica (NMO), and acute disseminated encephalomyelitis (ADEM). The study of ferroptosis may provide a new understanding of demyelinating diseases and provide a novel therapeutic target for clinical treatment. Herein, we reviewed recent discoveries on mechanisms of ferroptosis, the effects of metabolic pathways on ferroptosis, and its involvement in CNS demyelinating diseases. Ferroptosis is the result of multiple biological pathways acting together as a newly discovered cell death program. The major metabolic pathways associated with ferroptosis susceptibility include iron metabolism, lipid metabolism, and amino acid metabolism. Ferroptosis plays a key role in the pathophysiology of central nervous system (CNS) demyelinating diseases. Blocking the process of iron death can reduce myelin damage and alleviate the neurological dysfunction caused by demyelinating diseases such as multiple sclerosis, neuromyelitis optica, and acute disseminated encephalomyelitis.
Ferroptosis is a newly discovered programmed cell death caused by intracellular iron excess and glutathione (GSH) system imbalance, resulting in fatal lipid peroxidation. It is different from necrosis, apoptosis, autophagy, and other forms of cell death. Accumulating evidences suggest that brain iron overload is involved in the pathogenesis of demyelinating diseases of the central nervous system (CNS), such as multiple sclerosis (MS), neuromyelitis optica (NMO), and acute disseminated encephalomyelitis (ADEM). The study of ferroptosis may provide a new understanding of demyelinating diseases and provide a novel therapeutic target for clinical treatment. Herein, we reviewed recent discoveries on mechanisms of ferroptosis, the effects of metabolic pathways on ferroptosis, and its involvement in CNS demyelinating diseases. image
Ferroptosis is a newly discovered programmed cell death caused by intracellular iron excess and glutathione (GSH) system imbalance, resulting in fatal lipid peroxidation. It is different from necrosis, apoptosis, autophagy, and other forms of cell death. Accumulating evidences suggest that brain iron overload is involved in the pathogenesis of demyelinating diseases of the central nervous system (CNS), such as multiple sclerosis (MS), neuromyelitis optica (NMO), and acute disseminated encephalomyelitis (ADEM). The study of ferroptosis may provide a new understanding of demyelinating diseases and provide a novel therapeutic target for clinical treatment. Herein, we reviewed recent discoveries on mechanisms of ferroptosis, the effects of metabolic pathways on ferroptosis, and its involvement in CNS demyelinating diseases.Ferroptosis is a newly discovered programmed cell death caused by intracellular iron excess and glutathione (GSH) system imbalance, resulting in fatal lipid peroxidation. It is different from necrosis, apoptosis, autophagy, and other forms of cell death. Accumulating evidences suggest that brain iron overload is involved in the pathogenesis of demyelinating diseases of the central nervous system (CNS), such as multiple sclerosis (MS), neuromyelitis optica (NMO), and acute disseminated encephalomyelitis (ADEM). The study of ferroptosis may provide a new understanding of demyelinating diseases and provide a novel therapeutic target for clinical treatment. Herein, we reviewed recent discoveries on mechanisms of ferroptosis, the effects of metabolic pathways on ferroptosis, and its involvement in CNS demyelinating diseases.
Author Guo, Shougang
Qin, Danqing
Wang, Chunjuan
Li, Dong
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Keywords iron overload
cell death
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iron balance disorder
multiple sclerosis
oxidative stress
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Snippet Ferroptosis is a newly discovered programmed cell death caused by intracellular iron excess and glutathione (GSH) system imbalance, resulting in fatal lipid...
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SubjectTerms Apoptosis
Autophagy
Cell death
Central Nervous System
Central Nervous System Diseases
Demyelinating diseases
Demyelination
Encephalomyelitis
Ferroptosis
Glutathione
Humans
Iron
iron balance disorder
Iron Overload
Lipid peroxidation
Lipids
Metabolic pathways
Multiple Sclerosis
Necrosis
Neuromyelitis
Neuromyelitis Optica
Oxidative stress
Pathogenesis
Peroxidation
Therapeutic targets
Title Ferroptosis and central nervous system demyelinating diseases
URI https://onlinelibrary.wiley.com/doi/abs/10.1111%2Fjnc.15831
https://www.ncbi.nlm.nih.gov/pubmed/37095635
https://www.proquest.com/docview/2828562938
https://www.proquest.com/docview/2806071622
Volume 165
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