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dc.contributor.author
Martins, Airton C.
dc.contributor.author
Virgolini, Miriam Beatriz
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Tinkov, Alexey A.
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Skalny, Anatoly V.
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Tirumala, Rohan P.
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Farina, Marcelo
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Santamaria, Abel
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Lu, Rongzhu
dc.contributor.author
Aschner, Michael
dc.date.available
2023-07-26T17:16:38Z
dc.date.issued
2022-04
dc.identifier.citation
Martins, Airton C.; Virgolini, Miriam Beatriz; Tinkov, Alexey A.; Skalny, Anatoly V.; Tirumala, Rohan P.; et al.; Iron overload and neurodegenerative diseases: What can we learn from Caenorhabditis elegans?; SAGE Publications; Toxicology Research and Application; 6; 4-2022; 1-9
dc.identifier.issn
2397-8473
dc.identifier.uri
http://hdl.handle.net/11336/205647
dc.description.abstract
Iron (Fe) is an essential trace element required for several physiological processes. It plays important roles in mitochondrial function, synthesis, and metabolism of the neurotransmitter, as well as oxygen transport. However, excess Fe can cause toxicity. Particularly, Fe overload may result in neurotoxicity, contributing to the development and progression of neurodegenerative diseases, although the molecular mechanisms underlying Fe-induced neurodegeneration have yet to be entirely understood. Alternative (non-rodent) experimental models have been pointed as important approaches to elucidate molecular and physiological events mediating Fe-induced pathology. Among such alternative strategies, an advantageous experimental worm-model system, Caenorhabditis elegans (C. elegans), has been used to investigate Fe-induced neurotoxicity and neurodegenerative disorders. Its genome has been fully sequenced, corroborating that it shares significant homology with mammalians, and has approximately 40% of human disease-related genes. As part of this review, we discuss studies using the C. elegans model to study molecular mechanisms such as oxidative stress, mitochondrial dysfunction, disturbed homeostasis, and its potential contribution to the study of metal-induced neurodegenerative diseases such as Parkinson’s disease (PD) and Alzheimer’s disease (AD).
dc.format
application/pdf
dc.language.iso
eng
dc.publisher
SAGE Publications
dc.rights
info:eu-repo/semantics/openAccess
dc.rights.uri
https://creativecommons.org/licenses/by-nc/2.5/ar/
dc.subject
IRON
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NEURODEGENERATION
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ALZHEIMER
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PARKINSON
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Toxicología
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Medicina Básica
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CIENCIAS MÉDICAS Y DE LA SALUD
dc.title
Iron overload and neurodegenerative diseases: What can we learn from Caenorhabditis elegans?
dc.type
info:eu-repo/semantics/article
dc.type
info:ar-repo/semantics/artículo
dc.type
info:eu-repo/semantics/publishedVersion
dc.date.updated
2023-07-07T18:42:24Z
dc.journal.volume
6
dc.journal.pagination
1-9
dc.journal.pais
Estados Unidos
dc.journal.ciudad
California
dc.description.fil
Fil: Martins, Airton C.. Albert Einstein College of Medicine; Estados Unidos
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Fil: Virgolini, Miriam Beatriz. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Farmacología Experimental de Córdoba. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas. Instituto de Farmacología Experimental de Córdoba; Argentina. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas. Departamento de Farmacología; Argentina
dc.description.fil
Fil: Tinkov, Alexey A.. IM Sechenov First Moscow State Medical University; Rusia. Yaroslavl State University; Rusia
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Fil: Skalny, Anatoly V.. K.G. Razumovsky Moscow State University of Technologies and Managemen; Rusia. IM Sechenov First Moscow State Medical University; Rusia
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Fil: Tirumala, Rohan P.. Cupertino High School; Estados Unidos
dc.description.fil
Fil: Farina, Marcelo. Universidade Federal de Santa Catarina; Brasil
dc.description.fil
Fil: Santamaria, Abel. Instituto Nacional de Neurología y Neurocirugía; México
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Fil: Lu, Rongzhu. Jiangsu University; China
dc.description.fil
Fil: Aschner, Michael. Albert Einstein College of Medicine; Estados Unidos
dc.journal.title
Toxicology Research and Application
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/https://journals.sagepub.com/doi/10.1177/23978473221091852
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/https://doi.org/10.1177/23978473221091852
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