Ferroptosis: Is it both cause and effect in refractory epilepsy?
- Autores
- Auzmendi, Jerónimo Andrés; Lazarowski, Alberto Jorge
- Año de publicación
- 2025
- Idioma
- inglés
- Tipo de recurso
- artículo
- Estado
- versión publicada
- Descripción
- All living beings, from microorganisms to plants, animals, and humans, require iron as an essential micronutrient for their lives. However, iron overload can constitute a scenario prone to damage to the organism, including oxidative stress, deterioration of cellular and subcellular membranes, and thus leading to cell death. This process involves unrestricted lipid peroxidation caused by the generation of reactive oxygen species (ROS) because of an abrupt increase in free Fe2+ in the cytoplasm, all of which leads to subsequent membrane damage and iron-dependent cell death, now known as “ferroptosis”. This process can be induced by convulsive stress, and conversely, inducing seizures, and in both situations under a context of neuroinflammation. In this critical review, we will highlight the most relevant aspects of this recently described mechanism, which has been studied little in epilepsy, its impact on the prognosis of the disease, and its effects on the development of central and/or peripheral comorbidities, including SUDEP (sudden unexpected death in epilepsy).
Fil: Auzmendi, Jerónimo Andrés. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay; Argentina. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Fisiopatología y Bioquímica Clínica; Argentina
Fil: Lazarowski, Alberto Jorge. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Fisiopatología y Bioquímica Clínica; Argentina - Materia
-
EPILEPSY
FERROPTOSIS
HEMOSIDERIN
IRON DEPOSITION - Nivel de accesibilidad
- acceso abierto
- Condiciones de uso
- https://creativecommons.org/licenses/by/2.5/ar/
- Repositorio
.jpg)
- Institución
- Consejo Nacional de Investigaciones Científicas y Técnicas
- OAI Identificador
- oai:ri.conicet.gov.ar:11336/279568
Ver los metadatos del registro completo
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Ferroptosis: Is it both cause and effect in refractory epilepsy?Auzmendi, Jerónimo AndrésLazarowski, Alberto JorgeEPILEPSYFERROPTOSISHEMOSIDERINIRON DEPOSITIONhttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3All living beings, from microorganisms to plants, animals, and humans, require iron as an essential micronutrient for their lives. However, iron overload can constitute a scenario prone to damage to the organism, including oxidative stress, deterioration of cellular and subcellular membranes, and thus leading to cell death. This process involves unrestricted lipid peroxidation caused by the generation of reactive oxygen species (ROS) because of an abrupt increase in free Fe2+ in the cytoplasm, all of which leads to subsequent membrane damage and iron-dependent cell death, now known as “ferroptosis”. This process can be induced by convulsive stress, and conversely, inducing seizures, and in both situations under a context of neuroinflammation. In this critical review, we will highlight the most relevant aspects of this recently described mechanism, which has been studied little in epilepsy, its impact on the prognosis of the disease, and its effects on the development of central and/or peripheral comorbidities, including SUDEP (sudden unexpected death in epilepsy).Fil: Auzmendi, Jerónimo Andrés. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay; Argentina. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Fisiopatología y Bioquímica Clínica; ArgentinaFil: Lazarowski, Alberto Jorge. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Fisiopatología y Bioquímica Clínica; ArgentinaOpen Exploration Publishing2025-06info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/279568Auzmendi, Jerónimo Andrés; Lazarowski, Alberto Jorge; Ferroptosis: Is it both cause and effect in refractory epilepsy?; Open Exploration Publishing; Exploration of Neuroscience; 4; 100692 ; 6-2025; 1-112834-5347CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://www.explorationpub.com/Journals/en/Article/100692info:eu-repo/semantics/altIdentifier/doi/10.37349/en.2025.100692info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2026-02-26T09:58:45Zoai:ri.conicet.gov.ar:11336/279568instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982026-02-26 09:58:45.467CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse |
| dc.title.none.fl_str_mv |
Ferroptosis: Is it both cause and effect in refractory epilepsy? |
| title |
Ferroptosis: Is it both cause and effect in refractory epilepsy? |
| spellingShingle |
Ferroptosis: Is it both cause and effect in refractory epilepsy? Auzmendi, Jerónimo Andrés EPILEPSY FERROPTOSIS HEMOSIDERIN IRON DEPOSITION |
| title_short |
Ferroptosis: Is it both cause and effect in refractory epilepsy? |
| title_full |
Ferroptosis: Is it both cause and effect in refractory epilepsy? |
| title_fullStr |
Ferroptosis: Is it both cause and effect in refractory epilepsy? |
| title_full_unstemmed |
Ferroptosis: Is it both cause and effect in refractory epilepsy? |
| title_sort |
Ferroptosis: Is it both cause and effect in refractory epilepsy? |
| dc.creator.none.fl_str_mv |
Auzmendi, Jerónimo Andrés Lazarowski, Alberto Jorge |
| author |
Auzmendi, Jerónimo Andrés |
| author_facet |
Auzmendi, Jerónimo Andrés Lazarowski, Alberto Jorge |
| author_role |
author |
| author2 |
Lazarowski, Alberto Jorge |
| author2_role |
author |
| dc.subject.none.fl_str_mv |
EPILEPSY FERROPTOSIS HEMOSIDERIN IRON DEPOSITION |
| topic |
EPILEPSY FERROPTOSIS HEMOSIDERIN IRON DEPOSITION |
| purl_subject.fl_str_mv |
https://purl.org/becyt/ford/3.1 https://purl.org/becyt/ford/3 |
| dc.description.none.fl_txt_mv |
All living beings, from microorganisms to plants, animals, and humans, require iron as an essential micronutrient for their lives. However, iron overload can constitute a scenario prone to damage to the organism, including oxidative stress, deterioration of cellular and subcellular membranes, and thus leading to cell death. This process involves unrestricted lipid peroxidation caused by the generation of reactive oxygen species (ROS) because of an abrupt increase in free Fe2+ in the cytoplasm, all of which leads to subsequent membrane damage and iron-dependent cell death, now known as “ferroptosis”. This process can be induced by convulsive stress, and conversely, inducing seizures, and in both situations under a context of neuroinflammation. In this critical review, we will highlight the most relevant aspects of this recently described mechanism, which has been studied little in epilepsy, its impact on the prognosis of the disease, and its effects on the development of central and/or peripheral comorbidities, including SUDEP (sudden unexpected death in epilepsy). Fil: Auzmendi, Jerónimo Andrés. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay; Argentina. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Fisiopatología y Bioquímica Clínica; Argentina Fil: Lazarowski, Alberto Jorge. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Fisiopatología y Bioquímica Clínica; Argentina |
| description |
All living beings, from microorganisms to plants, animals, and humans, require iron as an essential micronutrient for their lives. However, iron overload can constitute a scenario prone to damage to the organism, including oxidative stress, deterioration of cellular and subcellular membranes, and thus leading to cell death. This process involves unrestricted lipid peroxidation caused by the generation of reactive oxygen species (ROS) because of an abrupt increase in free Fe2+ in the cytoplasm, all of which leads to subsequent membrane damage and iron-dependent cell death, now known as “ferroptosis”. This process can be induced by convulsive stress, and conversely, inducing seizures, and in both situations under a context of neuroinflammation. In this critical review, we will highlight the most relevant aspects of this recently described mechanism, which has been studied little in epilepsy, its impact on the prognosis of the disease, and its effects on the development of central and/or peripheral comorbidities, including SUDEP (sudden unexpected death in epilepsy). |
| publishDate |
2025 |
| dc.date.none.fl_str_mv |
2025-06 |
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info:eu-repo/semantics/article info:eu-repo/semantics/publishedVersion http://purl.org/coar/resource_type/c_6501 info:ar-repo/semantics/articulo |
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article |
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publishedVersion |
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http://hdl.handle.net/11336/279568 Auzmendi, Jerónimo Andrés; Lazarowski, Alberto Jorge; Ferroptosis: Is it both cause and effect in refractory epilepsy?; Open Exploration Publishing; Exploration of Neuroscience; 4; 100692 ; 6-2025; 1-11 2834-5347 CONICET Digital CONICET |
| url |
http://hdl.handle.net/11336/279568 |
| identifier_str_mv |
Auzmendi, Jerónimo Andrés; Lazarowski, Alberto Jorge; Ferroptosis: Is it both cause and effect in refractory epilepsy?; Open Exploration Publishing; Exploration of Neuroscience; 4; 100692 ; 6-2025; 1-11 2834-5347 CONICET Digital CONICET |
| dc.language.none.fl_str_mv |
eng |
| language |
eng |
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info:eu-repo/semantics/altIdentifier/url/https://www.explorationpub.com/Journals/en/Article/100692 info:eu-repo/semantics/altIdentifier/doi/10.37349/en.2025.100692 |
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