Mechanisms of Modulation of Ferroptosis and Its Role in Central Nervous System Diseases

Tan, Qingyun; Fang, Yixuan; Gu, Qiong

doi:10.3389/fphar.2021.657033

Cited by 48 publications

(26 citation statements)

References 110 publications

(134 reference statements)

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“…Cystine is reduced to cysteine to participate in GSH synthesis by system Xc - ( 60 ). The transport process of this system does not require ATP, and it is mediated by the difference in the concentration of amino acids presenting on both sides of the cell membrane ( 61 ). GSH is a tripeptide comprising glutamate, cysteine, and glycine.…”

Section: Molecular Mechanisms Of Cell Ferroptosismentioning

confidence: 99%

Molecular Mechanisms of Ferroptosis and Its Roles in Hematologic Malignancies

2021

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Cell death is essential for the normal metabolism of human organisms. Ferroptosis is a unique regulated cell death (RCD) mode characterized by excess accumulation of iron-dependent lipid peroxide and reactive oxygen species (ROS) compared with other well-known programmed cell death modes. It has been currently recognized that ferroptosis plays a rather important role in the occurrence, development, and treatment of traumatic brain injury, stroke, acute kidney injury, liver damage, ischemia–reperfusion injury, tumor, etc. Of note, ferroptosis may be explained by the expression of various molecules and signaling components, among which iron, lipid, and amino acid metabolism are the key regulatory mechanisms of ferroptosis. Meanwhile, tumor cells of hematological malignancies, such as leukemia, lymphoma, and multiple myeloma (MM), are identified to be sensitive to ferroptosis. Targeting potential regulatory factors in the ferroptosis pathway may promote or inhibit the disease progression of these malignancies. In this review, a systematic summary was conducted on the key molecular mechanisms of ferroptosis and the current potential relationships of ferroptosis with leukemia, lymphoma, and MM. It is expected to provide novel potential therapeutic approaches and targets for hematological malignancies.

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Section: Molecular Mechanisms Of Cell Ferroptosismentioning

confidence: 99%

Molecular Mechanisms of Ferroptosis and Its Roles in Hematologic Malignancies

2021

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“…As the name suggests, this programmed cell death pathway is dependent on iron, and is induced by the oxidation of polyunsaturated fatty acids (PUFAs) that are present in lipid bilayer membranes. Iron has been described to act as a catalyst in the Fenton reaction (where H 2 O 2 is converted to ·OH radicals), triggering a free-radical chain reaction and resulting in PUFA oxidation or degradation [ 72 ]. The iron-dependent oxidation of PUFAs causes mitochondrial alterations and cell membrane damage, which promotes cell death.…”

Section: Definition Of Oxidative Stress and Inflammationmentioning

confidence: 99%

Inherited Retinal Dystrophies: Role of Oxidative Stress and Inflammation in Their Physiopathology and Therapeutic Implications

et al. 2022

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Inherited retinal dystrophies (IRDs) are a large group of genetically and clinically heterogeneous diseases characterized by the progressive degeneration of the retina, ultimately leading to loss of visual function. Oxidative stress and inflammation play fundamental roles in the physiopathology of these diseases. Photoreceptor cell death induces an inflammatory state in the retina. The activation of several molecular pathways triggers different cellular responses to injury, including the activation of microglia to eliminate debris and recruit inflammatory cells from circulation. Therapeutical options for IRDs are currently limited, although a small number of patients have been successfully treated by gene therapy. Many other therapeutic strategies are being pursued to mitigate the deleterious effects of IRDs associated with oxidative metabolism and/or inflammation, including inhibiting reactive oxygen species’ accumulation and inflammatory responses, and blocking autophagy. Several compounds are being tested in clinical trials, generating great expectations for their implementation. The present review discusses the main death mechanisms that occur in IRDs and the latest therapies that are under investigation.

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“…According to models of cultured hippocampal slices of rat organs, ferroptosis was implicated to be the driving factor of neuronal death ( Dixon et al, 2012 ). Recent studies have linked ferroptosis to common diseases involving neuronal injury, such as stroke, Amyotrophic Lateral Sclerosis, Alzheimer’s disease and Parkinson’s disease ( Chen et al, 2021 ; Tan et al, 2021 ). It has also confirmed that ferroptosis exists and plays an important role in SCI.…”

Section: Tlr4 Signalingmentioning

confidence: 99%

Strategies for Biomaterial-Based Spinal Cord Injury Repair via the TLR4-NF-κB Signaling Pathway

Shen

Cheng

et al. 2022

Front. Bioeng. Biotechnol.

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The repair and motor functional recovery after spinal cord injury (SCI) has remained a clinical challenge. Injury-induced gliosis and inflammation lead to a physical barrier and an extremely inhibitory microenvironment, which in turn hinders the recovery of SCI. TLR4-NF-κB is a classic implant-related innate immunomodulation signaling pathway and part of numerous biomaterial-based treatment strategies for SCI. Numerous experimental studies have demonstrated that the regulation of TLR4-NF-κB signaling pathway plays an important role in the alleviation of inflammatory responses, the modulation of autophagy, apoptosis and ferroptosis, and the enhancement of anti-oxidative effect post-SCI. An increasing number of novel biomaterials have been fabricated as scaffolds and carriers, loaded with phytochemicals and drugs, to inhibit the progression of SCI through regulation of TLR4-NF-κB. This review summarizes the empirical strategies for the recovery after SCI through individual or composite biomaterials that mediate the TLR4-NF-κB signaling pathway.

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Mechanisms of Modulation of Ferroptosis and Its Role in Central Nervous System Diseases

Cited by 48 publications

References 110 publications

Molecular Mechanisms of Ferroptosis and Its Roles in Hematologic Malignancies

Molecular Mechanisms of Ferroptosis and Its Roles in Hematologic Malignancies

Inherited Retinal Dystrophies: Role of Oxidative Stress and Inflammation in Their Physiopathology and Therapeutic Implications

Strategies for Biomaterial-Based Spinal Cord Injury Repair via the TLR4-NF-κB Signaling Pathway

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