Ferroptosis: mechanisms, biology and role in disease
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 ha...
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| Published in | Nature reviews. Molecular cell biology Vol. 22; no. 4; pp. 266 - 282 |
|---|---|
| Main Authors | , , |
| Format | Journal Article |
| Language | English |
| Published |
London
Nature Publishing Group UK
01.04.2021
Nature Publishing Group |
| Subjects | |
| Online Access | Get full text |
| ISSN | 1471-0072 1471-0080 1471-0080 |
| DOI | 10.1038/s41580-020-00324-8 |
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| Abstract | 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.
Ferroptosis is a form of regulated cell death driven by iron-dependent phospholipid peroxidation. Since its formal identification in 2012, multiple studies have addressed molecular mechanisms, regulation and functions of ferroptosis, associating this cell death modality with various pathologies, but also proposing its roles in normal physiology and potential for therapeutic targeting. |
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| AbstractList | The research field of ferroptosis has been enjoying 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 events, including redox homeostasis, iron handling, mitochondrial activity, and metabolism of amino acids, lipids and sugars, in addition to numerous signaling pathways relevant to disease. Intriguingly, therapy-resistant cancer cells, particularly those of the mesenchymal state and prone to metastasis, are exquisitely vulnerable to ferroptosis. Further, numerous organ injuries and degenerative pathologies are driven by ferroptosis. As such, pharmacological modulation of ferroptosis, via both its induction and inhibition, holds great potential for the treatment of drug-resistant cancers, ischemic organ injuries, and other degenerative diseases linked to overwhelming lipid peroxidation. In this Review, we seek to provide an extensive and critical analysis of the current understanding of the molecular mechanisms and regulatory networks of ferroptosis, the potential physiological functions of ferroptosis in tumor suppression and immune surveillance, and its pathological roles and potential for therapeutics. Importantly, as in all rapidly evolving new research areas, issues and confusions exist due to misconceptions and inappropriate use of experimental tools – this Review also tries to address these issues and to provide practical guidelines. Finally, we discuss important concepts and pressing questions that should be a focus of future ferroptosis research. 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. 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.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. 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.Ferroptosis is a form of regulated cell death driven by iron-dependent phospholipid peroxidation. Since its formal identification in 2012, multiple studies have addressed molecular mechanisms, regulation and functions of ferroptosis, associating this cell death modality with various pathologies, but also proposing its roles in normal physiology and potential for therapeutic targeting. 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. Ferroptosis is a form of regulated cell death driven by iron-dependent phospholipid peroxidation. Since its formal identification in 2012, multiple studies have addressed molecular mechanisms, regulation and functions of ferroptosis, associating this cell death modality with various pathologies, but also proposing its roles in normal physiology and potential for therapeutic targeting. |
| Audience | Academic |
| Author | Conrad, Marcus Stockwell, Brent R. Jiang, Xuejun |
| AuthorAffiliation | 3 Institute of Metabolism and Cell Death, Helmholtz Zentrum München, Neuherberg, Germany 2 Department of Biological Sciences and Department of Chemistry, Columbia University, New York, NY 10027, USA 1 Cell Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA 4 Pirogov Russian National Research Medical University, Moscow, Russia |
| AuthorAffiliation_xml | – name: 3 Institute of Metabolism and Cell Death, Helmholtz Zentrum München, Neuherberg, Germany – name: 2 Department of Biological Sciences and Department of Chemistry, Columbia University, New York, NY 10027, USA – name: 1 Cell Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA – name: 4 Pirogov Russian National Research Medical University, Moscow, Russia |
| Author_xml | – sequence: 1 givenname: Xuejun orcidid: 0000-0002-8670-3828 surname: Jiang fullname: Jiang, Xuejun email: jiangx@mskcc.org organization: Cell Biology Program, Memorial Sloan Kettering Cancer Center – sequence: 2 givenname: Brent R. orcidid: 0000-0002-3532-3868 surname: Stockwell fullname: Stockwell, Brent R. email: bstockwell@columbia.edu organization: Department of Biological Sciences, Columbia University, Department of Chemistry, Columbia University – sequence: 3 givenname: Marcus orcidid: 0000-0003-1140-5612 surname: Conrad fullname: Conrad, Marcus email: marcus.conrad@helmholtz-muenchen.de organization: Institute of Metabolism and Cell Death, Helmholtz Zentrum München, Laboratory of Experimental Oncology, Pirogov Russian National Research Medical University |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/33495651$$D View this record in MEDLINE/PubMed |
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| Snippet | 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,... The research field of ferroptosis has been enjoying exponential growth over the past few years, since the term was coined in 2012. This unique modality of cell... |
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| SubjectTerms | 631/80/304 631/80/82 Amino acids Animals Apoptosis Biochemistry Biomedical and Life Sciences Cancer Cancer Research Cell Biology Cell death Cell research Degenerative diseases Developmental Biology Disease susceptibility Drug resistance Experimental methods Ferroptosis Ferroptosis - genetics Gene Regulatory Networks - genetics Health aspects Homeostasis Humans Immunosurveillance Injuries Iron Life Sciences Lipid metabolism Lipid Peroxidation Lipids Mesenchyme Metabolic pathways Metastases Methods Mitochondria Molecular modelling Molecular targeted therapy Mortality Neoplasms - genetics Oxidation-Reduction Peroxidation Phospholipids Physiology Reproducibility of Results Review Article Signal transduction Stem Cells Sugar Therapeutic targets Tumors |
| Title | Ferroptosis: mechanisms, biology and role in disease |
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