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Neuronal ferroptosis after intracerebral hemorrhage
Intracerebral hemorrhage (ICH) is a devastating form of stroke with high rates of morbidity, mortality, and disability. It induces cell death that is responsible for the secondary brain injury (SBI). The underlying mechanism of SBI after ICH is still unclear, and whether it is related to iron overlo...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Frontiers Media S.A.
2022
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9388724/ https://www.ncbi.nlm.nih.gov/pubmed/35992267 http://dx.doi.org/10.3389/fmolb.2022.966478 |
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author | Ren, Siying Chen, Yue Wang, Likun Wu, Guofeng |
author_facet | Ren, Siying Chen, Yue Wang, Likun Wu, Guofeng |
author_sort | Ren, Siying |
collection | PubMed |
description | Intracerebral hemorrhage (ICH) is a devastating form of stroke with high rates of morbidity, mortality, and disability. It induces cell death that is responsible for the secondary brain injury (SBI). The underlying mechanism of SBI after ICH is still unclear, and whether it is related to iron overload is worthy to be discussed. Ferroptosis is an iron-dependent non-apoptotic modes of cell death and plays a particularly important role in the occurrence and progression of ICH. Many ICH-induced regulators and signalling pathways of ferroptosis have been reported as promising targets for treating ICH. In this article, we review the definition, characteristics, and inhibition methods of neuronal ferroptosis caused by iron deposition after ICH, and review the biomarkers for ferroptosis. |
format | Online Article Text |
id | pubmed-9388724 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-93887242022-08-20 Neuronal ferroptosis after intracerebral hemorrhage Ren, Siying Chen, Yue Wang, Likun Wu, Guofeng Front Mol Biosci Molecular Biosciences Intracerebral hemorrhage (ICH) is a devastating form of stroke with high rates of morbidity, mortality, and disability. It induces cell death that is responsible for the secondary brain injury (SBI). The underlying mechanism of SBI after ICH is still unclear, and whether it is related to iron overload is worthy to be discussed. Ferroptosis is an iron-dependent non-apoptotic modes of cell death and plays a particularly important role in the occurrence and progression of ICH. Many ICH-induced regulators and signalling pathways of ferroptosis have been reported as promising targets for treating ICH. In this article, we review the definition, characteristics, and inhibition methods of neuronal ferroptosis caused by iron deposition after ICH, and review the biomarkers for ferroptosis. Frontiers Media S.A. 2022-08-05 /pmc/articles/PMC9388724/ /pubmed/35992267 http://dx.doi.org/10.3389/fmolb.2022.966478 Text en Copyright © 2022 Ren, Chen, Wang and Wu. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Molecular Biosciences Ren, Siying Chen, Yue Wang, Likun Wu, Guofeng Neuronal ferroptosis after intracerebral hemorrhage |
title | Neuronal ferroptosis after intracerebral hemorrhage |
title_full | Neuronal ferroptosis after intracerebral hemorrhage |
title_fullStr | Neuronal ferroptosis after intracerebral hemorrhage |
title_full_unstemmed | Neuronal ferroptosis after intracerebral hemorrhage |
title_short | Neuronal ferroptosis after intracerebral hemorrhage |
title_sort | neuronal ferroptosis after intracerebral hemorrhage |
topic | Molecular Biosciences |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9388724/ https://www.ncbi.nlm.nih.gov/pubmed/35992267 http://dx.doi.org/10.3389/fmolb.2022.966478 |
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