Evidence for TGF-β1/Nrf2 Signaling Crosstalk in a Cuprizone Model of Multiple Sclerosis

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dc.contributor.authorGuevara, Coram
dc.contributor.authorVicencio, Sinay C.
dc.contributor.authorPizarro, Ignacio S.
dc.contributor.authorVillavicencio-Tejo, Francisca
dc.contributor.authorQuintanilla, Rodrigo A.
dc.contributor.authorAstudillo, Pablo
dc.contributor.authorAmpuero, Estibaliz
dc.contributor.authorVaras, Rodrigo
dc.contributor.authorOrellana, Juan A.
dc.contributor.authorOrtiz, Fernando C.
dc.date.accessioned2025-01-20T16:09:08Z
dc.date.available2025-01-20T16:09:08Z
dc.date.issued2024
dc.description.abstractMultiple sclerosis (MS) is a chronic and degenerative disease that impacts central nervous system (CNS) function. One of the major characteristics of the disease is the presence of regions lacking myelin and an oxidative and inflammatory environment. TGF-beta 1 and Nrf2 proteins play a fundamental role in different oxidative/inflammatory processes linked to neurodegenerative diseases such as MS. The evidence from different experimental settings has demonstrated a TGF-beta 1-Nrf2 signaling crosstalk under pathological conditions. However, this possibility has not been explored in experimental models of MS. Here, by using the cuprizone-induced demyelination model of MS, we report that the in vivo pharmacological blockage of the TGF-beta 1 receptor reduced Nrf2, catalase, and TGF beta-1 protein levels in the demyelination phase of cuprizone administration. In addition, ATP production, locomotor function and cognitive performance were diminished by the treatment. Altogether, our results provide evidence for a crosstalk between TGF-beta 1 and Nrf2 signaling pathways under CNS demyelination, highlighting the importance of the antioxidant cellular response of neurodegenerative diseases such as MS.
dc.fuente.origenWOS
dc.identifier.doi10.3390/antiox13080914
dc.identifier.eissn2076-3921
dc.identifier.urihttps://doi.org/10.3390/antiox13080914
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/90133
dc.identifier.wosidWOS:001305855000001
dc.issue.numero8
dc.language.isoen
dc.revistaAntioxidants
dc.rightsacceso restringido
dc.subjectmultiple sclerosis
dc.subjectdemyelination
dc.subjectneuroinflammation
dc.subjectoxidative stress
dc.subjecttransforming growth factor beta 1 TGF-beta 1
dc.subjectNrf2
dc.subject.ods03 Good Health and Well-being
dc.subject.odspa03 Salud y bienestar
dc.titleEvidence for TGF-β1/Nrf2 Signaling Crosstalk in a Cuprizone Model of Multiple Sclerosis
dc.typeartículo
dc.volumen13
sipa.indexWOS
sipa.trazabilidadWOS;2025-01-12
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