Neurodegeneration in Multiple Sclerosis: The Role of Nrf2-Dependent Pathways

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dc.article.number1146
dc.catalogadorgjm
dc.contributor.authorMaldonado, Paloma P.
dc.contributor.authorGuevara, Coram
dc.contributor.authorOlesen, Margrethe A.
dc.contributor.authorOrellana Roca, Juan Andrés
dc.contributor.authorQuintanilla, Rodrigo A.
dc.contributor.authorOrtiz, Fernando C.
dc.date.accessioned2024-10-16T15:56:56Z
dc.date.available2024-10-16T15:56:56Z
dc.date.issued2022
dc.description.abstractMultiple sclerosis (MS) encompasses a chronic, irreversible, and predominantly immune-mediated disease of the central nervous system that leads to axonal degeneration, neuronal death, and several neurological symptoms. Although various immune therapies have reduced relapse rates and the severity of symptoms in relapsing-remitting MS, there is still no cure for this devastating disease. In this brief review, we discuss the role of mitochondria dysfunction in the progression of MS, focused on the possible role of Nrf2 signaling in orchestrating the impairment of critical cellular and molecular aspects such as reactive oxygen species (ROS) management, under neuroinflammation and neurodegeneration in MS. In this scenario, we propose a new potential downstream signaling of Nrf2 pathway, namely the opening of hemichannels and pannexons. These large-pore channels are known to modulate glial/neuronal function and ROS production as they are permeable to extracellular Ca2+ and release potentially harmful transmitters to the synaptic cleft. In this way, the Nrf2 dysfunction impairs not only the bioenergetics and metabolic properties of glial cells but also the proper antioxidant defense and energy supply that they provide to neurons.
dc.description.funderFondo Nacional de Desarrollo Cientifico y Tecnologico (FONDECYT)
dc.fechaingreso.objetodigital2024-10-16
dc.fuente.origenORCID
dc.identifier.doi10.3390/antiox11061146
dc.identifier.eissn2076-3921
dc.identifier.urihttps://doi.org/10.3390/antiox11061146
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/88264
dc.identifier.wosidWOS:000818297500001
dc.information.autorucEscuela de Medicina; Orellana Roca, Juan Andrés; 0000-0003-4076-207X; 126007
dc.issue.numero6
dc.language.isoen
dc.nota.accesocontenido completo
dc.revistaAntioxidants
dc.rightsacceso abierto
dc.rights.licenseCC BY 4.0 Attribution 4.0 International Deed
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/
dc.subjectMultiple sclerosis
dc.subjectNrf2-dependent pathways
dc.subjectNeuroinflammation
dc.subjectPannexin-1
dc.subjectGlial cells
dc.subjectReactive oxygen species
dc.subjectMitochondria
dc.subject.ddc610
dc.subject.deweyMedicina y saludes_ES
dc.subject.ods03 Good health and well-being
dc.subject.odspa03 Salud y bienestar
dc.titleNeurodegeneration in Multiple Sclerosis: The Role of Nrf2-Dependent Pathways
dc.typeartículo
dc.volumen11
sipa.codpersvinculados126007
sipa.trazabilidadORCID;2024-10-14
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