For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
7
views
176
references
 Top references
cited by
3
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      870
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Targeting Ferroptosis in Bone-Related Diseases: Facts and Perspectives

      review-article

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Ferroptosis is a new cell fate decision discovered in recent years. Unlike apoptosis, autophagy or pyroptosis, ferroptosis is characterized by iron-dependent lipid peroxidation and mitochondrial morphological changes. Ferroptosis is involved in a variety of physiological and pathological processes. Since its discovery, ferroptosis has been increasingly studied concerning bone-related diseases. In this review, we focus on the latest research progress and prospects, summarize the regulatory mechanisms of ferroptosis, and discuss the role of ferroptosis in the pathogenesis of bone-related diseases, such as osteoporosis (OP), osteoarthritis (OA), rheumatoid arthritis (RA), and osteosarcoma (OS), as well as its therapeutic potential.

          Related collections

          Most cited references176

          • Record: found
          • Abstract: found
          • Article: not found

          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.
          Article 0 comments Cited 4921 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            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.
            Article 0 comments Cited 1475 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              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.
              Article 0 comments Cited 1397 times – based on 0 reviews     Review now
                Bookmark
                All references

                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): 18 October 2023
                Publication date Collection: 2023
                Volume: 16
                Pages: 4661-4677
                Affiliations
                [1 ]Department of Orthopaedics, Chengdu Xinhua Hospital , Chengdu, 610000, People’s Republic of China
                [2 ]School of Medical and Life Sciences, Chengdu University of Traditional Chinese Medicine , Chengdu, 610000, People’s Republic of China
                [3 ]Department of Orthopaedics, The First People’s Hospital of Longquanyi District , Chengdu, 610000, People’s Republic of China
                [4 ]School of Ophthalmology, Chengdu University of Traditional Chinese Medicine , Chengdu, 610000, People’s Republic of China
                [5 ]Sichuan Judicial and Police Officers Professional College , Deyang, 618000, People’s Republic of China
                [6 ]Affiliated Hospital of North Sichuan Medical College , Nanchong, 637000, People’s Republic of China
                Author notes
                Correspondence: Houdong Zuo, Department of Orthopaedics, Chengdu Xinhua Hospital , Chengdu, 610000, People’s Republic of China, Email xhyyzhd@163.com
                Liuyan Chen, School of Medical and Life Sciences, Chengdu University of Traditional Chinese Medicine , Chengdu, 610000, People’s Republic of China, Email Lycheecly@163.com
                [*]

                These authors contributed equally to this work

                Article
                Publisher ID: 432111
                DOI: 10.2147/JIR.S432111
                PMC ID: 10590556
                PubMed ID: 37872954
                SO-VID: 38e584f4-3056-4725-966e-b6d2661e1a15
                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 : 24 July 2023
                Date accepted : 12 October 2023
                Page count
                Figures: 3, Tables: 1, References: 176, Pages: 17
                Funding
                Funded by: Project of Chengdu Municipal Health Commission;
                The work was founded by Project of Chengdu Municipal Health Commission (2022573).
                Categories
                Subject: Review

                ScienceOpen disciplines: Immunology
                Keywords: ferroptosis,cell death,iron accumulation,lipid peroxidation,bone-related diseases
                Data availability:
                ScienceOpen disciplines: Immunology
                Keywords: ferroptosis, cell death, iron accumulation, lipid peroxidation, bone-related diseases

                Comments

                Comment on this article

                scite_

                Similar content870

                See all similar

                Cited by3

                See all cited by

                Most referenced authors3,240

                See all reference authors