dc.creatorRuiz Cortés, Zulma Tatiana
dc.creatorfourcade, Stéphane
dc.creatorMorató, Laia
dc.creatorParameswaran, Janani
dc.creatorRuiz, Montserrat
dc.creatorJové, Ariona
dc.creatorNaudí, Alba
dc.creatorMartínez Redondo, Paloma
dc.creatorDierssen, Mara
dc.creatorFerrer, Isidre
dc.creatorVillarroya, Francesc
dc.creatorPamplona, Reinald
dc.creatorVaquero, Alejandro
dc.creatorPortero Otín, Manel
dc.creatorPujol, Aurora
dc.date2023-04-01T20:30:19Z
dc.date2023-04-01T20:30:19Z
dc.date2017
dc.date.accessioned2024-04-23T14:12:11Z
dc.date.available2024-04-23T14:12:11Z
dc.identifierFourcade S, Morató L, Parameswaran J, Ruiz M, Ruiz-Cortés T, Jové M, Naudí A, Martínez-Redondo P, Dierssen M, Ferrer I, Villarroya F, Pamplona R, Vaquero A, Portero-Otín M, Pujol A. Loss of SIRT2 leads to axonal degeneration and locomotor disability associated with redox and energy imbalance. Aging Cell. 2017 Dec;16(6):1404-1413. doi: 10.1111/acel.12682.
dc.identifier1474-9718
dc.identifierhttps://hdl.handle.net/10495/34420
dc.identifier10.1111/acel.12682
dc.identifier1474-9726
dc.identifier.urihttps://repositorioslatinoamericanos.uchile.cl/handle/2250/9229217
dc.descriptionABSTRACT: Sirtuin 2 (SIRT2) is a member of a family of NAD+ -dependent histone deacetylases (HDAC) that play diverse roles in cellular metabolism and especially for aging process. SIRT2 is located in the nucleus, cytoplasm, and mitochondria, is highly expressed in the central nervous system (CNS), and has been reported to regulate a variety of processes including oxidative stress, genome integrity, and myelination. However, little is known about the role of SIRT2 in the nervous system specifically during aging. Here, we show that middle-aged, 13-month-old mice lacking SIRT2 exhibit locomotor dysfunction due to axonal degeneration, which was not present in young SIRT2 mice. In addition, these Sirt2 / mice exhibit mitochondrial depletion resulting in energy failure, and redox dyshomeostasis. Our results provide a novel link between SIRT2 and physiological aging impacting the axonal compartment of the central nervous system, while supporting a major role for SIRT2 in orchestrating its metabolic regulation. This underscores the value of SIRT2 as a therapeutic target in the most prevalent neurodegenerative diseases that undergo with axonal degeneration associated with redox and energetic dyshomeostasis. Key words: aging; axonal degeneration; mitochondria; redox dyshomeostasis; sirtuin.
dc.descriptionCOL0066561
dc.format10
dc.formatapplication/pdf
dc.formatapplication/pdf
dc.languageeng
dc.publisherWiley
dc.publisherBiogénesis
dc.publisherOxford, Inglaterra
dc.relationAging Cell.
dc.rightsinfo:eu-repo/semantics/openAccess
dc.rightshttp://creativecommons.org/licenses/by/2.5/co/
dc.rightshttp://purl.org/coar/access_right/c_abf2
dc.rightshttps://creativecommons.org/licenses/by/4.0/
dc.subjectEnvejecimiento
dc.subjectAging
dc.subjectAxones
dc.subjectAxons
dc.subjectADN Mitocondrial
dc.subjectDNA, Mitochondrial
dc.subjectMetabolismo Energético
dc.subjectEnergy Metabolism
dc.subjectRatones
dc.subjectMice
dc.subjectRatones Endogámicos C57BL
dc.subjectMice, Inbred C57BL
dc.subjectRatones Noqueados
dc.subjectMice, Knockout
dc.subjectSirtuinas 2
dc.subjectSirtuins 2
dc.subjectEnfermedades Neurodegenerativas
dc.subjectNeurodegenerative Diseases
dc.titleLoss of SIRT2 leads to axonal degeneration and locomotor disability associated with redox and energy imbalance
dc.typeinfo:eu-repo/semantics/article
dc.typeinfo:eu-repo/semantics/publishedVersion
dc.typehttp://purl.org/coar/resource_type/c_2df8fbb1
dc.typehttps://purl.org/redcol/resource_type/ART
dc.typeArtículo de investigación


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