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      The Emerging Roles of Ferroptosis in Neonatal Diseases

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          Abstract

          Ferroptosis is a novel type of programmed cell death involved in many diseases’ pathological processes. Ferroptosis is characterized by lipid peroxidation, reactive oxygen species accumulation, and iron metabolism disorder. Newborns are susceptible to ferroptosis due to their special physiological state, which is prone to abnormal iron metabolism and the accumulation of reactive oxygen species. Recent studies have linked ferroptosis to a variety of diseases in the neonatal period (including hypoxic-ischemic encephalopathy, bronchopulmonary dysplasia, and necrotizing enterocolitis). Ferroptosis may become an effective target for the treatment of neonatal-related diseases. In this review, the ferroptosis molecular mechanism, metabolism characteristics of iron and reactive oxygen species in infants, the relationship between ferroptosis and common infant disorders, and the treatment of infant diseases targeted for ferroptosis are systematically summarized.

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          Most cited references139

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          Ferroptosis: an iron-dependent form of nonapoptotic cell death.

          Scott J. Dixon, Kathryn Lemberg, Michael Lamprecht … (2012)
          Nonapoptotic forms of cell death may facilitate the selective elimination of some tumor cells or be activated in specific pathological states. The oncogenic RAS-selective lethal small molecule erastin triggers a unique iron-dependent form of nonapoptotic cell death that we term ferroptosis. Ferroptosis is dependent upon intracellular iron, but not other metals, and is morphologically, biochemically, and genetically distinct from apoptosis, necrosis, and autophagy. We identify the small molecule ferrostatin-1 as a potent inhibitor of ferroptosis in cancer cells and glutamate-induced cell death in organotypic rat brain slices, suggesting similarities between these two processes. Indeed, erastin, like glutamate, inhibits cystine uptake by the cystine/glutamate antiporter (system x(c)(-)), creating a void in the antioxidant defenses of the cell and ultimately leading to iron-dependent, oxidative death. Thus, activation of ferroptosis results in the nonapoptotic destruction of certain cancer cells, whereas inhibition of this process may protect organisms from neurodegeneration. Copyright © 2012 Elsevier Inc. All rights reserved.
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            Ferroptosis: mechanisms, biology and role in disease

            Xuejun Jiang, Brent Stockwell, Marcus Conrad (2021)
            The research field of ferroptosis has seen exponential growth over the past few years, since the term was coined in 2012. This unique modality of cell death, driven by iron-dependent phospholipid peroxidation, is regulated by multiple cellular metabolic pathways, including redox homeostasis, iron handling, mitochondrial activity and metabolism of amino acids, lipids and sugars, in addition to various signalling pathways relevant to disease. Numerous organ injuries and degenerative pathologies are driven by ferroptosis. Intriguingly, therapy-resistant cancer cells, particularly those in the mesenchymal state and prone to metastasis, are exquisitely vulnerable to ferroptosis. As such, pharmacological modulation of ferroptosis, via both its induction and its inhibition, holds great potential for the treatment of drug-resistant cancers, ischaemic organ injuries and other degenerative diseases linked to extensive lipid peroxidation. In this Review, we provide a critical analysis of the current molecular mechanisms and regulatory networks of ferroptosis, the potential physiological functions of ferroptosis in tumour suppression and immune surveillance, and its pathological roles, together with a potential for therapeutic targeting. Importantly, as in all rapidly evolving research areas, challenges exist due to misconceptions and inappropriate experimental methods. This Review also aims to address these issues and to provide practical guidelines for enhancing reproducibility and reliability in studies of ferroptosis. Finally, we discuss important concepts and pressing questions that should be the focus of future ferroptosis research.
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              ACSL4 dictates ferroptosis sensitivity by shaping cellular lipid composition.

              Sebastian Doll, Bettina Proneth, Yulia Tyurina … (2017)
              Ferroptosis is a form of regulated necrotic cell death controlled by glutathione peroxidase 4 (GPX4). At present, mechanisms that could predict sensitivity and/or resistance and that may be exploited to modulate ferroptosis are needed. We applied two independent approaches-a genome-wide CRISPR-based genetic screen and microarray analysis of ferroptosis-resistant cell lines-to uncover acyl-CoA synthetase long-chain family member 4 (ACSL4) as an essential component for ferroptosis execution. Specifically, Gpx4-Acsl4 double-knockout cells showed marked resistance to ferroptosis. Mechanistically, ACSL4 enriched cellular membranes with long polyunsaturated ω6 fatty acids. Moreover, ACSL4 was preferentially expressed in a panel of basal-like breast cancer cell lines and predicted their sensitivity to ferroptosis. Pharmacological targeting of ACSL4 with thiazolidinediones, a class of antidiabetic compound, ameliorated tissue demise in a mouse model of ferroptosis, suggesting that ACSL4 inhibition is a viable therapeutic approach to preventing ferroptosis-related diseases.
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                Author and article information

                Journal
                Journal ID (nlm-ta): J Inflamm Res
                Journal ID (iso-abbrev): J Inflamm Res
                Journal ID (publisher-id): jir
                Title: Journal of Inflammation Research
                Publisher: Dove
                ISSN (Electronic): 1178-7031
                Publication date (Electronic): 26 June 2023
                Publication date Collection: 2023
                Volume: 16
                Pages: 2661-2674
                Affiliations
                [1 ]Department of Neonatology, Fujian Maternity and Child Health Hospital, Affiliated Hospital of Fujian Medical University , Fuzhou, People’s Republic of China
                [2 ]Key Laboratory of Stomatology of Fujian Province, School and Hospital of Stomatology, Fujian Medical University , Fuzhou, People’s Republic of China
                Author notes
                Correspondence: Changyi Yang, Department of Neonatology, Fujian Maternity and Child Health Hospital, Affiliated Hospital of Fujian Medical University , Fuzhou, 350001, People’s Republic of China, Tel +86 15959000599, Fax +86 87279676, Email yangchangyi@fjmu.edu.cn
                Author information
                http://orcid.org/0000-0002-7896-1472
                http://orcid.org/0000-0003-2345-4040
                http://orcid.org/0009-0006-9764-2975
                Article
                Publisher ID: 414316
                DOI: 10.2147/JIR.S414316
                PMC ID: 10312340
                PubMed ID: 37396013
                SO-VID: 6242842c-500c-4f85-ba2a-d38b3fa22c30
                Copyright © © 2023 Chen et al.
                License:

                This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms ( https://www.dovepress.com/terms.php).

                History
                Date received : 26 March 2023
                Date accepted : 13 June 2023
                Page count
                Figures: 2, Tables: 1, References: 139, Pages: 14
                Categories
                Subject: Review

                ScienceOpen disciplines: Immunology
                Keywords: ferroptosis,neonatal disease,reactive oxygen species,iron metabolism,lipid peroxidation
                Data availability:
                ScienceOpen disciplines: Immunology
                Keywords: ferroptosis, neonatal disease, reactive oxygen species, iron metabolism, lipid peroxidation

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