Oxidative stress and impaired oligodendrocyte precursor cell differentiation in neurological disorders

Vista sencilla de ítem
dc.contributor.authorSpaas, Jan
dc.contributor.authorVan Veggel, Lieve
dc.contributor.authorSchepers, Melissa
dc.contributor.authorTiane, Assia
dc.contributor.authorVan Horssen, Jack
dc.contributor.authorWilson, David M.
dc.contributor.authorMoya, Pablo
dc.contributor.authorPiccart, Elisabeth
dc.contributor.authorHellings, Niels
dc.contributor.authorEijnde, Bert O.
dc.contributor.authorDerave, Wim
dc.contributor.authorSchreiber, Rudy
dc.contributor.authorVanmierlo, Tim
dc.date.accessioned2022-11-30T02:47:01Z
dc.date.available2022-11-30T02:47:01Z
dc.date.issued2021
dc.description.abstractOligodendrocyte precursor cells (OPCs) account for 5% of the resident parenchymal central nervous system glial cells. OPCs are not only a back-up for the loss of oligodendrocytes that occurs due to brain injury or infammation-induced demyelination (remyelination) but are also pivotal in plastic processes such as learning and memory (adaptive myelination). OPC diferentiation into mature myelinating oligodendrocytes is controlled by a complex transcriptional network and depends on high metabolic and mitochondrial demand. Mounting evidence shows that OPC dysfunction, culminating in the lack of OPC diferentiation, mediates the progression of neurodegenerative disorders such as multiple sclerosis, Alzheimer’s disease and Parkinson’s disease. Importantly, neurodegeneration is characterised by oxidative and carbonyl stress, which may primarily afect OPC plasticity due to the high metabolic demand and a limited antioxidant capacity associated with this cell type.The underlying mechanisms of how oxidative/carbonyl stress disrupt OPC diferentiation remain enigmatic and a focus of current research eforts. This review proposes a role for oxidative/carbonyl stress in interfering with the transcriptional and metabolic changes required for OPC diferentiation. In particular, oligodendrocyte (epi)geneticsen_ES
dc.description.abstractcellular defence and repair responses, mitochondrial signalling and respiration, and lipid metabolism represent key mechanisms how oxidative/carbonyl stress may hamper OPC diferentiation in neurodegenerative disorders. Understanding how oxidative/carbonyl stress impacts OPC function may pave the way for future OPC-targeted treatment strategies in neurodegenerative disorders.en_ES
dc.facultadFacultad de Cienciasen_ES
dc.file.nameSpaas_Oxi2021.pdf
dc.identifier.citationSpaas, J.; van Veggel, L.; Schepers, M. et al. Oxidative stress and impaired oligodendrocyte precursor cell differentiation in neurological disorders. Cell. Mol. Life Sci. 78, 4615–4637 (2021). https://doi.org/10.1007/s00018-021-03802-0en_ES
dc.identifier.doihttps://doi.org/10.1007/s00018-021-03802-0
dc.identifier.urihttp://repositoriobibliotecas.uv.cl/handle/uvscl/7551
dc.languageen
dc.publisherSpringer
dc.rightsOpen Access. This article is licensed under a Creative Commons Attribution 4.0 International
dc.sourceCellular and Molecular Life Sciences
dc.subjectOLIGODENDROCYTE PRECURSOR CELLen_ES
dc.subjectOXIDATIVE STRESSen_ES
dc.subjectCARBONYL STRESSen_ES
dc.subjectNEURODEGENERATIONen_ES
dc.subjectMYELINATIONen_ES
dc.titleOxidative stress and impaired oligodendrocyte precursor cell differentiation in neurological disorders
dc.typeArticulo
uv.departamentoInstituto de Fisiologia

Archivos

Bloque original
Mostrando 1 - 1 de 1
Miniatura
Nombre:
Spaas_Oxi2021.pdf
Tamaño:
1.41 MB
Formato:
Adobe Portable Document Format
Descargar

Colecciones

Artículos investigadores UV