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Cell Metabolism and Oxidative Stress in the Process of Ferroptosis...
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Cell Metabolism and Oxidative Stress in the Process of Ferroptosis in Different Human Disease

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Metabolism".

Deadline for manuscript submissions: closed (15 February 2023) | Viewed by 16474

Special Issue Editors

Dr. Maura Poli

E-Mail Website
Guest Editor
Department of Molecular and Translational Medicine, University of Brescia, 25121 Brescia, Italy
Interests: iron metabolism; hepcidin regulation; heparin; ferroptosis; tumor
Special Issues, Collections and Topics in MDPI journals
Dr. Michela Asperti

E-Mail Website
Guest Editor
Department of Molecular and Translational Medicine, University of Brescia, 25121 Brescia, Italy
Interests: iron metabolism; hepcidin regulation; heparan sulfate; heparin; ferroptosis; tumor

Special Issue Information

Dear Colleagues,

Ferroptosis is a form of regulated cell death dependent on iron, reactive oxygen species and characterized by the accumulation of lipid peroxides due to the reduction of antioxidant machinery, mainly connected with glutathione peroxidase (Gpx4) activity. Since its discovery in 2012, many research studies have been published focusing on the mechanisms of ferroptosis, its induction in tumor cells, which is carried out by many chemical compounds, or its prevention in various human disorders, such as in neurodegeneration or ischemia reperfusion injury. Recently, it has been reported that the SARS-COV2 infection leads to multiorgan damage that shows signs of ferroptosis.

Thus, the study of ferroptosis is a currently developing area of research, and its induction or prevention seems to be a new promising therapeutic approach. Nowadays, a lot of information is available related to ferroptosis, and the three peculiar hallmarks of this cell death have been defined, such as the oxidation of PUFA-PLs, the presence of redox-active iron, defective or inhibited lipid peroxide repair system and the cell-specific metabolism, which confers sensitivity or resistance toward this process. However, some aspects are not yet deeply investigated, and many open questions are still unsolved. This Special Issue aims to provide a complete overview of what is already known about the ferroptotic process together with the different points not yet completely understood, looking at the process as both a usable approach to suppress tumor growth and a mechanism to be suppressed to solve some human diseases. 

Dr. Maura Poli
Dr. Michela Asperti
Guest Editors

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. Cells is an international peer-reviewed open access semimonthly 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 2700 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

  • ferroptosis
  • iron
  • ferritinophagy
  • metabolism
  • lipid peroxidation
  • antioxidant machinery
  • free radical biology
  • cancer
  • neurodegeneration
  • cardiovascular disorders
  • SARS-COV2

Published Papers (6 papers)

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Research

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16 pages, 5393 KiB  
Article
Myo-Inositol Supplementation Alleviates Cisplatin-Induced Acute Kidney Injury via Inhibition of Ferroptosis
by Huiyue Qi, Fei Deng, Yinghuai Wang, Hao Zhang, Yashpal S. Kanwar and Yingbo Dai
Cells 2023, 12(1), 16; https://doi.org/10.3390/cells12010016 - 21 Dec 2022
Cited by 7 | Viewed by 2004
Abstract
Myo-inositol, a carbocyclic sugar, is believed to be relevant to renal pathobiology since the kidney is the major site for its catabolism. Its role in acute kidney injury (AKI) has not been fully investigated. Ferroptosis, a unique form of regulated cell death, [...] Read more.
Myo-inositol, a carbocyclic sugar, is believed to be relevant to renal pathobiology since the kidney is the major site for its catabolism. Its role in acute kidney injury (AKI) has not been fully investigated. Ferroptosis, a unique form of regulated cell death, is involved in various types of renal injuries. The relevance of myo-inositol with respect to the process of ferroptosis has not been explored either. Herein, our current exploratory studies revealed that supplementation of myo-inositol attenuates cisplatin-induced injury in cultured Boston University mouse proximal tubular (BUMPT) cells and renal tubules in vivo. Moreover, our studies unraveled that metabolic parameters pertaining to ferroptosis were disrupted in cisplatin-treated proximal tubular cells, which were seemingly remedied by the administration of myo-inositol. Mechanistically, we noted that cisplatin treatment led to the up-regulation of NOX4, a key enzyme relevant to ferroptosis, which was normalized by the administration of myo-inositol. Furthermore, we observed that changes in the NOX4 expression induced by cisplatin or myo-inositol were modulated by carboxy-terminus of Hsc70-interacting protein (CHIP), an E3 ubiquitin ligase. Taken together, our investigation suggests that myo-inositol promotes CHIP-mediated ubiquitination of NOX4 to decelerate the process of ferroptosis, leading to the amelioration of cisplatin-induced AKI. Full article
(This article belongs to the Special Issue Cell Metabolism and Oxidative Stress in the Process of Ferroptosis in Different Human Disease)
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26 pages, 10525 KiB  
Article
Ferroptosis-Related Gene GCLC Is a Novel Prognostic Molecular and Correlates with Immune Infiltrates in Lung Adenocarcinoma
by Lianxiang Luo, Zhentao Zhang, Yanmin Weng and Jiayan Zeng
Cells 2022, 11(21), 3371; https://doi.org/10.3390/cells11213371 - 25 Oct 2022
Cited by 6 | Viewed by 1913
Abstract
Ferroptosis, a newly discovered iron-dependent type of cell death, has been found to play a crucial role in the depression of tumorigenesis. However, the prognostic value of ferroptosis-related genes (FRGs) in lung adenocarcinoma (LUAD) remains to be further elucidated. Differential expression analysis and [...] Read more.
Ferroptosis, a newly discovered iron-dependent type of cell death, has been found to play a crucial role in the depression of tumorigenesis. However, the prognostic value of ferroptosis-related genes (FRGs) in lung adenocarcinoma (LUAD) remains to be further elucidated. Differential expression analysis and univariate Cox regression analysis were utilized in this study to search for FRGs that were associated with the prognosis of LUAD patients. The influences of candidate markers on LUAD cell proliferation, migration, and ferroptosis were evaluated by CCK8, colony formation, and functional experimental assays in association with ferroptosis. To predict the prognosis of LUAD patients, we constructed a predictive signature comprised of six FRGs. We discovered a critical gene (GCLC) after intersecting the prognostic analysis results of all aspects, and its high expression was associated with a bad prognosis in LUAD. Correlation research revealed that GCLC was related to a variety of clinical information from LUAD patients. At the same time, in the experimental verification, we found that GCLC expression was upregulated in LUAD cell lines, and silencing GCLC accelerated ferroptosis and decreased LUAD cell proliferation and invasion. Taken together, this study established a novel ferroptosis-related gene signature and discovered a crucial gene, GCLC, that might be a new prognostic biomarker of LUAD patients, as well as provide a potential therapeutic target for LUAD patients. Full article
(This article belongs to the Special Issue Cell Metabolism and Oxidative Stress in the Process of Ferroptosis in Different Human Disease)
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13 pages, 1226 KiB  
Article
Methionine Deprivation Reveals the Pivotal Roles of Cell Cycle Progression in Ferroptosis That Is Induced by Cysteine Starvation
by Takujiro Homma, Sho Kobayashi and Junichi Fujii
Cells 2022, 11(10), 1603; https://doi.org/10.3390/cells11101603 - 10 May 2022
Cited by 15 | Viewed by 2641
Abstract
Ferroptosis, a type of iron-dependent necrotic cell death, is triggered by the accumulation of excessive lipid peroxides in cells. Glutathione (GSH), a tripeptide redox molecule that contains a cysteine (Cys) unit in the center, plays a pivotal role in protection against ferroptosis. When [...] Read more.
Ferroptosis, a type of iron-dependent necrotic cell death, is triggered by the accumulation of excessive lipid peroxides in cells. Glutathione (GSH), a tripeptide redox molecule that contains a cysteine (Cys) unit in the center, plays a pivotal role in protection against ferroptosis. When the transsulfuration pathway is activated, the sulfur atom of methionine (Met) is utilized to generate Cys, which can then suppress Cys-starvation-induced ferroptosis. In the current study, we cultured HeLa cells in Met- and/or cystine (an oxidized Cys dimer)- deprived medium and investigated the roles of Met in ferroptosis execution. The results indicate that, in the absence of cystine or Met, ferroptosis or cell cycle arrest, respectively, occurred. Contrary to our expectations, however, the simultaneous deprivation of both Met and cystine failed to induce ferroptosis, although the intracellular levels of Cys and GSH were maintained at low levels. Supplementation with S-adenosylmethionine (SAM), a methyl group donor that is produced during the metabolism of Met, caused the cell cycle progression to resume and lipid peroxidation and the subsequent induction of ferroptosis was also restored under conditions of Met/cystine double deprivation. DNA methylation appeared to be involved in the resumption in the SAM-mediated cell cycle because its downstream metabolite S-adenosylhomocysteine failed to cause either cell cycle progression or ferroptosis to be induced. Taken together, our results suggest that elevated lipid peroxidation products that are produced during cell cycle progression are involved in the execution of ferroptosis under conditions of Cys starvation. Full article
(This article belongs to the Special Issue Cell Metabolism and Oxidative Stress in the Process of Ferroptosis in Different Human Disease)
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Review

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22 pages, 2194 KiB  
Review
Ferroptosis Regulated by Hypoxia in Cells
by Xiangnan Zheng, Yuqiong Liang and Cen Zhang
Cells 2023, 12(7), 1050; https://doi.org/10.3390/cells12071050 - 30 Mar 2023
Cited by 8 | Viewed by 3252
Abstract
Ferroptosis is an oxidative damage-related, iron-dependent regulated cell death with intracellular lipid peroxide accumulation, which is associated with many physiological and pathological processes. It exhibits unique features that are morphologically, biochemically, and immunologically distinct from other regulated cell death forms. Ferroptosis is regulated [...] Read more.
Ferroptosis is an oxidative damage-related, iron-dependent regulated cell death with intracellular lipid peroxide accumulation, which is associated with many physiological and pathological processes. It exhibits unique features that are morphologically, biochemically, and immunologically distinct from other regulated cell death forms. Ferroptosis is regulated by iron metabolism, lipid metabolism, anti-oxidant defense systems, as well as various signal pathways. Hypoxia, which is found in a group of physiological and pathological conditions, can affect multiple cellular functions by activation of the hypoxia-inducible factor (HIF) signaling and other mechanisms. Emerging evidence demonstrated that hypoxia regulates ferroptosis in certain cell types and conditions. In this review, we summarize the basic mechanisms and regulations of ferroptosis and hypoxia, as well as the regulation of ferroptosis by hypoxia in physiological and pathological conditions, which may contribute to the numerous diseases therapies. Full article
(This article belongs to the Special Issue Cell Metabolism and Oxidative Stress in the Process of Ferroptosis in Different Human Disease)
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25 pages, 2605 KiB  
Review
New Insights into the Role of Ferroptosis in Cardiovascular Diseases
by Anna Maria Fratta Pasini, Chiara Stranieri, Fabiana Busti, Edoardo Giuseppe Di Leo, Domenico Girelli and Luciano Cominacini
Cells 2023, 12(6), 867; https://doi.org/10.3390/cells12060867 - 10 Mar 2023
Cited by 10 | Viewed by 2604
Abstract
Cardiovascular diseases (CVDs) are the principal cause of disease burden and death worldwide. Ferroptosis is a new form of regulated cell death mainly characterized by altered iron metabolism, increased polyunsaturated fatty acid peroxidation by reactive oxygen species, depletion of glutathione and inactivation of [...] Read more.
Cardiovascular diseases (CVDs) are the principal cause of disease burden and death worldwide. Ferroptosis is a new form of regulated cell death mainly characterized by altered iron metabolism, increased polyunsaturated fatty acid peroxidation by reactive oxygen species, depletion of glutathione and inactivation of glutathione peroxidase 4. Recently, a series of studies have indicated that ferroptosis is involved in the death of cardiac and vascular cells and has a key impact on the mechanisms leading to CVDs such as ischemic heart disease, ischemia/reperfusion injury, cardiomyopathies, and heart failure. In this article, we reviewed the molecular mechanism of ferroptosis and the current understanding of the pathophysiological role of ferroptosis in ischemic heart disease and in some cardiomyopathies. Moreover, the comprehension of the machinery governing ferroptosis in vascular cells and cardiomyocytes may provide new insights into preventive and therapeutic strategies in CVDs. Full article
(This article belongs to the Special Issue Cell Metabolism and Oxidative Stress in the Process of Ferroptosis in Different Human Disease)
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18 pages, 398 KiB  
Review
Progress and Setbacks in Translating a Decade of Ferroptosis Research into Clinical Practice
by Friedrich Alexander von Samson-Himmelstjerna, Benedikt Kolbrink, Theresa Riebeling, Ulrich Kunzendorf and Stefan Krautwald
Cells 2022, 11(14), 2134; https://doi.org/10.3390/cells11142134 - 06 Jul 2022
Cited by 4 | Viewed by 2706
Abstract
Ten years after its initial description, ferroptosis has emerged as the most intensely studied entity among the non-apoptotic forms of regulated cell death. The molecular features of ferroptotic cell death and its functional role have been characterized in vitro and in an ever-growing [...] Read more.
Ten years after its initial description, ferroptosis has emerged as the most intensely studied entity among the non-apoptotic forms of regulated cell death. The molecular features of ferroptotic cell death and its functional role have been characterized in vitro and in an ever-growing number of animal studies, demonstrating that it exerts either highly detrimental or, depending on the context, occasionally beneficial effects on the organism. Consequently, two contrary therapeutic approaches are being explored to exploit our detailed understanding of this cell death pathway: the inhibition of ferroptosis to limit organ damage in disorders such as drug-induced toxicity or ischemia-reperfusion injury, and the induction of ferroptosis in cancer cells to ameliorate anti-tumor strategies. However, the path from basic science to clinical utility is rocky. Emphasizing ferroptosis inhibition, we review the success and failures thus far in the translational process from basic research in the laboratory to the treatment of patients. Full article
(This article belongs to the Special Issue Cell Metabolism and Oxidative Stress in the Process of Ferroptosis in Different Human Disease)
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