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Antioxidants
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Iron Metabolism, Redox Balance and Neurological Diseases
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Iron Metabolism, Redox Balance and Neurological Diseases

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: closed (30 April 2023) | Viewed by 25146

Printed Edition Available!
A printed edition of this Special Issue is available here.

Special Issue Editor

Prof. Dr. Yan-Zhong Chang

E-Mail Website
Guest Editor
Laboratory of Molecular Iron Metabolism, College of Life Science, Hebei Normal University, Shijiazhuang 050024, China
Interests: iron metabolism; iron misregulation; redox imbalance; Parkinson's disease; Alzheimer's disease; stroke; mental and emotional disorders; preparation and safety evaluation of brain-targeted nanomedicines
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The misregulation of brain iron homeostasis can lead to severe pathological changes in the neurological system. Iron deficiency slows the development of the neural system and causes mental and emotional disorders, while iron overload is closely related to neurodegenerative diseases such as Alzheimer’s disease, Parkinson’s disease and cerebral ischemia. Free iron can elicit the generation of reactive oxygen species (ROS) due to its ability to catalyze the Fenton reaction, which contributes significantly to the pathophysiological mechanisms of neurological diseases. On the other hand, some free radicals also play an important role in the normal function of cells as signaling molecules. Iron misregulation and redox imbalance are the keys to the occurrence and development of many neurological diseases. Therefore, iron metabolism and redox regulation as targets have become or will become a great potential solution for the treatment of neurological diseases. This Special Issue aims to collect the latest research findings and review articles with great advances on the mechanisms or treatments of neurological diseases related to iron misregulation/redox imbalance, and to stimulate new thinking in the field of iron metabolism, redox balance and neurological diseases.

Prof. Dr. Yan-Zhong Chang
Guest Editor

Manuscript Submission Information

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Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Antioxidants is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • iron metabolism
  • redox
  • Alzheimer's disease
  • Parkinson's disease
  • stroke
  • antioxidants
  • brain-targeted nanomedicines

Published Papers (11 papers)

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Editorial

Jump to: Research, Review, Other

4 pages, 213 KiB  
Editorial
Iron Metabolism, Redox Balance and Neurological Diseases
by Guofen Gao and Yan-Zhong Chang
Antioxidants 2023, 12(9), 1721; https://doi.org/10.3390/antiox12091721 - 5 Sep 2023
Cited by 1 | Viewed by 684
Abstract
Iron is essential for life, and the dysregulation of iron homeostasis can lead to severe pathological changes in the neurological system [...] Full article
(This article belongs to the Special Issue Iron Metabolism, Redox Balance and Neurological Diseases)

Research

Jump to: Editorial, Review, Other

16 pages, 3541 KiB  
Article
Deubiquitylase OTUD3 Mediates Endoplasmic Reticulum Stress through Regulating Fortilin Stability to Restrain Dopaminergic Neurons Apoptosis
by Ling Chen, Xuejie Huan, Fengju Jia, Zhen Zhang, Mingxia Bi, Lin Fu, Xixun Du, Xi Chen, Chunling Yan, Qian Jiao and Hong Jiang
Antioxidants 2023, 12(4), 809; https://doi.org/10.3390/antiox12040809 - 26 Mar 2023
Cited by 2 | Viewed by 1455
Abstract
OTU domain-containing protein 3 (OTUD3) knockout mice exhibited loss of nigral dopaminergic neurons and Parkinsonian symptoms. However, the underlying mechanisms are largely unknown. In this study, we observed that the inositol-requiring enzyme 1α (IRE1α)-induced endoplasmic reticulum (ER) stress was involved in this process. [...] Read more.
OTU domain-containing protein 3 (OTUD3) knockout mice exhibited loss of nigral dopaminergic neurons and Parkinsonian symptoms. However, the underlying mechanisms are largely unknown. In this study, we observed that the inositol-requiring enzyme 1α (IRE1α)-induced endoplasmic reticulum (ER) stress was involved in this process. We found that the ER thickness and the expression of protein disulphide isomerase (PDI) were increased, and the apoptosis level was elevated in the dopaminergic neurons of OTUD3 knockout mice. These phenomena were ameliorated by ER stress inhibitor tauroursodeoxycholic acid (TUDCA) treatment. The ratio of p-IRE1α/IRE1α, and the expression of X-box binding protein 1-spliced (XBP1s) were remarkably increased after OTUD3 knockdown, which was inhibited by IRE1α inhibitor STF-083010 treatment. Moreover, OTUD3 regulated the ubiquitination level of Fortilin through binding with the OTU domain. OTUD3 knockdown resulted in a decrease in the interaction ability of IRE1α with Fortilin and finally enhanced the activity of IRE1α. Taken together, we revealed that OTUD3 knockout-induced injury of dopaminergic neurons might be caused by activating IRE1α signaling in ER stress. These findings demonstrated that OTUD3 played a critical role in dopaminergic neuron neurodegeneration, which provided new evidence for the multiple and tissue-dependent functions of OTUD3. Full article
(This article belongs to the Special Issue Iron Metabolism, Redox Balance and Neurological Diseases)
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26 pages, 15890 KiB  
Article
Inhibiting NLRP3 Inflammasome Activation by CY-09 Helps to Restore Cerebral Glucose Metabolism in 3×Tg-AD Mice
by Shuangxue Han, Zhijun He, Xia Hu, Xiaoqian Li, Kaixin Zheng, Yingying Huang, Peng Xiao, Qingguo Xie, Jiazuan Ni and Qiong Liu
Antioxidants 2023, 12(3), 722; https://doi.org/10.3390/antiox12030722 - 15 Mar 2023
Cited by 9 | Viewed by 2053
Abstract
The reduction of the cerebral glucose metabolism is closely related to the activation of the NOD-like receptor protein 3 (NLRP3) inflammasome in Alzheimer’s disease (AD); however, its underlying mechanism remains unclear. In this paper, 18F-flurodeoxyglucose positron emission tomography was used to trace [...] Read more.
The reduction of the cerebral glucose metabolism is closely related to the activation of the NOD-like receptor protein 3 (NLRP3) inflammasome in Alzheimer’s disease (AD); however, its underlying mechanism remains unclear. In this paper, 18F-flurodeoxyglucose positron emission tomography was used to trace cerebral glucose metabolism in vivo, along with Western blotting and immunofluorescence assays to examine the expression and distribution of associated proteins. Glucose and insulin tolerance tests were carried out to detect insulin resistance, and the Morris water maze was used to test the spatial learning and memory ability of the mice. The results show increased NLRP3 inflammasome activation, elevated insulin resistance, and decreased glucose metabolism in 3×Tg-AD mice. Inhibiting NLRP3 inflammasome activation using CY-09, a specific inhibitor for NLRP3, may restore cerebral glucose metabolism by increasing the expression and distribution of glucose transporters and enzymes and attenuating insulin resistance in AD mice. Moreover, CY-09 helps to improve AD pathology and relieve cognitive impairment in these mice. Although CY-09 has no significant effect on ferroptosis, it can effectively reduce fatty acid synthesis and lipid peroxidation. These findings provide new evidence for NLRP3 inflammasome as a therapeutic target for AD, suggesting that CY-09 may be a potential drug for the treatment of this disease. Full article
(This article belongs to the Special Issue Iron Metabolism, Redox Balance and Neurological Diseases)
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15 pages, 4579 KiB  
Article
Stimulation of Hepatic Ferritinophagy Mitigates Irp2 Depletion-Induced Anemia
by Yutong Liu, Yuxuan Li, Liu Yang, Jiaqi Shen, Hongting Zhao, Weichen Dong, Yanzhong Chang, Tong Qiao and Kuanyu Li
Antioxidants 2023, 12(3), 566; https://doi.org/10.3390/antiox12030566 - 24 Feb 2023
Cited by 2 | Viewed by 1690
Abstract
Background: Iron regulatory proteins (IRPs) maintain cellular iron homeostasis. Due to aberrant tissue-iron distribution, Irp2-deficient mice suffer microcytic anemia and neurodegeneration, while iron overload occurs in the liver and intestine. We previously found that Irp2 deficiency-induced Hif2 plays an important role in [...] Read more.
Background: Iron regulatory proteins (IRPs) maintain cellular iron homeostasis. Due to aberrant tissue-iron distribution, Irp2-deficient mice suffer microcytic anemia and neurodegeneration, while iron overload occurs in the liver and intestine. We previously found that Irp2 deficiency-induced Hif2 plays an important role in neurodegeneration. Methods: To test the role of Hif2 in Irp2 deficiency-induced anemia, we used Irp2 global knockout mice. Following Hif2 inhibition, routine blood tests, iron availability in bone marrow, histological assays, and biochemical analysis were performed to assess anemia improvement and tissue iron distribution. Results: We found that Hif2 inhibition improved anemia. The increased iron bioavailability for erythropoiesis was mainly derived from hepatic iron release, and secondly from enhanced intestinal absorption. We further demonstrate that nuclear receptor coactivator 4 (Ncoa4) was upregulated for iron release via the process of ferritinophagy. The released iron was utilized not only for intracellular Fe-S biogenesis but also for erythropoiesis after being exported from the liver to circulation. The hepatic iron export reduced hepcidin expression to further support iron absorption through the hepcidin-ferroportin axis to alleviate intestinal iron overload. Conclusion: Irp2 not only regulates cellular iron homeostasis but also tissue iron distribution by managing the involvement of Hif2-Ncoa4. Full article
(This article belongs to the Special Issue Iron Metabolism, Redox Balance and Neurological Diseases)
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18 pages, 4432 KiB  
Article
Mitochondrial-Targeted Antioxidant MitoQ-Mediated Autophagy: A Novel Strategy for Precise Radiation Protection
by Xingting Bao, Xiongxiong Liu, Qingfeng Wu, Fei Ye, Zheng Shi, Dan Xu, Jinhua Zhang, Zhihui Dou, Guomin Huang, Hong Zhang and Chao Sun
Antioxidants 2023, 12(2), 453; https://doi.org/10.3390/antiox12020453 - 10 Feb 2023
Cited by 3 | Viewed by 2224
Abstract
Radiotherapy (RT) is one of the most effective cancer treatments. However, successful radiation protection for normal tissue is a clinical challenge. Our previous study observed that MitoQ, a mitochondria-targeted antioxidant, was adsorbed to the inner mitochondrial membrane and remained the cationic moiety in [...] Read more.
Radiotherapy (RT) is one of the most effective cancer treatments. However, successful radiation protection for normal tissue is a clinical challenge. Our previous study observed that MitoQ, a mitochondria-targeted antioxidant, was adsorbed to the inner mitochondrial membrane and remained the cationic moiety in the intermembrane space. The positive charges in MitoQ restrained the activity of respiratory chain complexes and decreased proton production. Therefore, a pseudo-mitochondrial membrane potential (PMMP) was developed via maintenance of exogenous positive charges. This study identified that PMMP constructed by MitoQ could effectively inhibit mitochondrial respiration within normal cells, disrupt energy metabolism, and activate adenosine 5′-monophosphate (AMP)-activated protein kinase (AMPK) signaling to induce autophagy. As such, it could not lead to starvation-induced autophagy among tumor cells due to the different energy phenotypes between normal and tumor cells (normal cells depend on mitochondrial respiration for energy supply, while tumor cells rely on aerobic glycolysis). Therefore, we successfully protected the normal cells from radiation-induced damage without affecting the tumor-killing efficacy of radiation by utilizing selective autophagy. MitoQ-constructed PMMP provides a new therapeutic strategy for specific radiation protection. Full article
(This article belongs to the Special Issue Iron Metabolism, Redox Balance and Neurological Diseases)
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16 pages, 3265 KiB  
Article
CHIR99021 Maintenance of the Cell Stemness by Regulating Cellular Iron Metabolism
by Yingying Han, Yong He, Xiaofang Jin, Jiayi Xie, Peng Yu, Guofen Gao, Shiyang Chang, Jianhua Zhang and Yan-Zhong Chang
Antioxidants 2023, 12(2), 377; https://doi.org/10.3390/antiox12020377 - 4 Feb 2023
Cited by 4 | Viewed by 1867
Abstract
CHIR99021 is an aminopyrimidine derivative, which can efficiently inhibit the activity of glycogen synthesis kinase 3α (GSK-3α) and GSK-3β. As an essential component of stem cell culture medium, it plays an important role in maintaining cell stemness. However, the mechanism of its role [...] Read more.
CHIR99021 is an aminopyrimidine derivative, which can efficiently inhibit the activity of glycogen synthesis kinase 3α (GSK-3α) and GSK-3β. As an essential component of stem cell culture medium, it plays an important role in maintaining cell stemness. However, the mechanism of its role is not fully understood. In the present study, we first found that removal of CHIR99021 from embryonic stem cell culture medium reduced iron storage in mouse embryonic stem cells (mESCs). CHIR99021-treated Neuro-2a cells led to an upregulation of ferritin expression and an increase in intracellular iron levels, along with GSK3β inhibition and Wnt/GSK-3β/β-catenin pathway activation. In addition, iron treatment activated the classical Wnt pathway by affecting the expression of β-catenin in the Neuro-2a cells. Our data link the role of iron in the maintenance of cell stemness via the Wnt/GSK-3β/β-catenin signaling pathway, and identify intermediate molecules, including Steap1, Bola2, and Kdm6bos, which may mediate the upregulation of ferritin expression by CHIR99021. These findings reveal novel mechanisms of the maintenance of cell stemness and differentiation and provide a theoretical basis for the development of new strategies in stem cell treatment in disease. Full article
(This article belongs to the Special Issue Iron Metabolism, Redox Balance and Neurological Diseases)
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Review

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34 pages, 3068 KiB  
Review
Brain Iron Metabolism, Redox Balance and Neurological Diseases
by Guofen Gao, Linhao You, Jianhua Zhang, Yan-Zhong Chang and Peng Yu
Antioxidants 2023, 12(6), 1289; https://doi.org/10.3390/antiox12061289 - 16 Jun 2023
Cited by 14 | Viewed by 1936
Abstract
The incidence of neurological diseases, such as Parkinson’s disease, Alzheimer’s disease and stroke, is increasing. An increasing number of studies have correlated these diseases with brain iron overload and the resulting oxidative damage. Brain iron deficiency has also been closely linked to neurodevelopment. [...] Read more.
The incidence of neurological diseases, such as Parkinson’s disease, Alzheimer’s disease and stroke, is increasing. An increasing number of studies have correlated these diseases with brain iron overload and the resulting oxidative damage. Brain iron deficiency has also been closely linked to neurodevelopment. These neurological disorders seriously affect the physical and mental health of patients and bring heavy economic burdens to families and society. Therefore, it is important to maintain brain iron homeostasis and to understand the mechanism of brain iron disorders affecting reactive oxygen species (ROS) balance, resulting in neural damage, cell death and, ultimately, leading to the development of disease. Evidence has shown that many therapies targeting brain iron and ROS imbalances have good preventive and therapeutic effects on neurological diseases. This review highlights the molecular mechanisms, pathogenesis and treatment strategies of brain iron metabolism disorders in neurological diseases. Full article
(This article belongs to the Special Issue Iron Metabolism, Redox Balance and Neurological Diseases)
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22 pages, 1973 KiB  
Review
The Interplay between Intracellular Iron Homeostasis and Neuroinflammation in Neurodegenerative Diseases
by Jaewang Lee and Dong-Hoon Hyun
Antioxidants 2023, 12(4), 918; https://doi.org/10.3390/antiox12040918 - 12 Apr 2023
Cited by 15 | Viewed by 3113
Abstract
Iron is essential for life. Many enzymes require iron for appropriate function. However, dysregulation of intracellular iron homeostasis produces excessive reactive oxygen species (ROS) via the Fenton reaction and causes devastating effects on cells, leading to ferroptosis, an iron-dependent cell death. In order [...] Read more.
Iron is essential for life. Many enzymes require iron for appropriate function. However, dysregulation of intracellular iron homeostasis produces excessive reactive oxygen species (ROS) via the Fenton reaction and causes devastating effects on cells, leading to ferroptosis, an iron-dependent cell death. In order to protect against harmful effects, the intracellular system regulates cellular iron levels through iron regulatory mechanisms, including hepcidin–ferroportin, divalent metal transporter 1 (DMT1)–transferrin, and ferritin–nuclear receptor coactivator 4 (NCOA4). During iron deficiency, DMT1–transferrin and ferritin–NCOA4 systems increase intracellular iron levels via endosomes and ferritinophagy, respectively. In contrast, repleting extracellular iron promotes cellular iron absorption through the hepcidin–ferroportin axis. These processes are regulated by the iron-regulatory protein (IRP)/iron-responsive element (IRE) system and nuclear factor erythroid 2-related factor 2 (Nrf2). Meanwhile, excessive ROS also promotes neuroinflammation by activating the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB). NF-κB forms inflammasomes, inhibits silent information regulator 2-related enzyme 1 (SIRT1), and induces pro-inflammatory cytokines (IL-6, TNF-α, and IL-1β). Furthermore, 4-hydroxy-2,3-trans-nonenal (4-HNE), the end-product of ferroptosis, promotes the inflammatory response by producing amyloid-beta (Aβ) fibrils and neurofibrillary tangles in Alzheimer’s disease, and alpha-synuclein aggregation in Parkinson’s disease. This interplay shows that intracellular iron homeostasis is vital to maintain inflammatory homeostasis. Here, we review the role of iron homeostasis in inflammation based on recent findings. Full article
(This article belongs to the Special Issue Iron Metabolism, Redox Balance and Neurological Diseases)
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14 pages, 838 KiB  
Review
Dysregulated Iron Homeostasis as Common Disease Etiology and Promising Therapeutic Target
by Bruce E. Holbein and Christian Lehmann
Antioxidants 2023, 12(3), 671; https://doi.org/10.3390/antiox12030671 - 9 Mar 2023
Cited by 6 | Viewed by 2629
Abstract
Iron is irreplaceably required for animal and human cells as it provides the activity center for a wide variety of essential enzymes needed for energy production, nucleic acid synthesis, carbon metabolism and cellular defense. However, iron is toxic when present in excess and [...] Read more.
Iron is irreplaceably required for animal and human cells as it provides the activity center for a wide variety of essential enzymes needed for energy production, nucleic acid synthesis, carbon metabolism and cellular defense. However, iron is toxic when present in excess and its uptake and storage must, therefore, be tightly regulated to avoid damage. A growing body of evidence indicates that iron dysregulation leading to excess quantities of free reactive iron is responsible for a wide range of otherwise discrete diseases. Iron excess can promote proliferative diseases such as infections and cancer by supplying iron to pathogens or cancer cells. Toxicity from reactive iron plays roles in the pathogenesis of various metabolic, neurological and inflammatory diseases. Interestingly, a common underlying aspect of these conditions is availability of excess reactive iron. This underpinning aspect provides a potential new therapeutic avenue. Existing hematologically used iron chelators to take up excess iron have shown serious limitations for use but new purpose-designed chelators in development show promise for suppressing microbial pathogen and cancer cell growth, and also for relieving iron-induced toxicity in neurological and other diseases. Hepcidin and hepcidin agonists are also showing promise for relieving iron dysregulation. Harnessing iron-driven reactive oxygen species (ROS) generation with ferroptosis has shown promise for selective destruction of cancer cells. We review biological iron requirements, iron regulation and the nature of iron dysregulation in various diseases. Current results pertaining to potential new therapies are also reviewed. Full article
(This article belongs to the Special Issue Iron Metabolism, Redox Balance and Neurological Diseases)
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19 pages, 1203 KiB  
Review
Ferroptosis and Its Potential Role in Glioma: From Molecular Mechanisms to Therapeutic Opportunities
by Yusong Luo, Guopeng Tian, Xiang Fang, Shengwei Bai, Guoqiang Yuan and Yawen Pan
Antioxidants 2022, 11(11), 2123; https://doi.org/10.3390/antiox11112123 - 28 Oct 2022
Cited by 11 | Viewed by 2539
Abstract
Glioma is the most common intracranial malignant tumor, and the current main standard treatment option is a combination of tumor surgical resection, chemotherapy and radiotherapy. Due to the terribly poor five-year survival rate of patients with gliomas and the high recurrence rate of [...] Read more.
Glioma is the most common intracranial malignant tumor, and the current main standard treatment option is a combination of tumor surgical resection, chemotherapy and radiotherapy. Due to the terribly poor five-year survival rate of patients with gliomas and the high recurrence rate of gliomas, some new and efficient therapeutic strategies are expected. Recently, ferroptosis, as a new form of cell death, has played a significant role in the treatment of gliomas. Specifically, studies have revealed key processes of ferroptosis, including iron overload in cells, occurrence of lipid peroxidation, inactivation of cysteine/glutathione antiporter system Xc− (xCT) and glutathione peroxidase 4 (GPX4). In the present review, we summarized the molecular mechanisms of ferroptosis and introduced the application and challenges of ferroptosis in the development and treatment of gliomas. Moreover, we highlighted the therapeutic opportunities of manipulating ferroptosis to improve glioma treatments, which may improve the clinical outcome. Full article
(This article belongs to the Special Issue Iron Metabolism, Redox Balance and Neurological Diseases)
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Other

15 pages, 1298 KiB  
Systematic Review
Coenzyme Q10 and Dementia: A Systematic Review
by Félix Javier Jiménez-Jiménez, Hortensia Alonso-Navarro, Elena García-Martín and José A. G. Agúndez
Antioxidants 2023, 12(2), 533; https://doi.org/10.3390/antiox12020533 - 20 Feb 2023
Cited by 10 | Viewed by 3988
Abstract
It is well known that coenzyme Q10 (CoQ10) has important antioxidant properties. Because one of the main mechanisms involved in the pathogenesis of Alzheimer’s disease (AD) and other neurodegenerative diseases is oxidative stress, analysis of the concentrations of CoQ10 [...] Read more.
It is well known that coenzyme Q10 (CoQ10) has important antioxidant properties. Because one of the main mechanisms involved in the pathogenesis of Alzheimer’s disease (AD) and other neurodegenerative diseases is oxidative stress, analysis of the concentrations of CoQ10 in different tissues of AD patients and with other dementia syndromes and the possible therapeutic role of CoQ10 in AD have been addressed in several studies. We performed a systematic review and a meta-analysis of these studies measuring tissue CoQ10 levels in patients with dementia and controls which showed that, compared with controls, AD patients had similar serum/plasma CoQ10 levels. We also revised the possible therapeutic effects of CoQ10 in experimental models of AD and other dementias (which showed important neuroprotective effects of coenzyme Q10) and in humans with AD, other dementias, and mild cognitive impairment (with inconclusive results). The potential role of CoQ10 treatment in AD and in improving memory in aged rodents shown in experimental models deserves future studies in patients with AD, other causes of dementia, and mild cognitive impairment. Full article
(This article belongs to the Special Issue Iron Metabolism, Redox Balance and Neurological Diseases)
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