ArticleAntioxidants (Basel, Switzerland)2024
Evidence for TGF-β1/Nrf2 Signaling Crosstalk in a Cuprizone Model of Multiple Sclerosis.
Article in Antioxidants (Basel, Switzerland), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Neuroprotective effects of glucotropaeolin as the major glucosinolate of cress seed on cuprizone-induced mouse model of multiple sclerosis.Biochemistry and biophysics reports · 2026Article
- Impact of Anti-CD20 Therapies on Cytokine, Chemokine and Adhesion Molecule Dynamics in Multiple Sclerosis: A Narrative Review.Neurology and therapy · 2026Review
- Connecting the Dots: Neurobiological Interplay Between Type 2 Diabetes and Alzheimer's Disease.International journal of molecular sciences · 2026Review
- Berberine protects against behavioral deficits, memory dysfunction, and callosal demyelination in cuprizone-intoxicated C57BL/6 mice.Iranian journal of basic medical sciences · 2026Article
- Synthesis and Evaluation of the Effects of Nanoparticles of Atorvastatin and Atorvastatin on Cuprizone-Induced Demyelination: Modulation of the Nrf2/NF-kB Signaling Pathway.Iranian journal of pharmaceutical research : IJPRArticle
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Multiple 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-β1 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-β1-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-β1 receptor reduced Nrf2, catalase, and TGFβ-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-β1 and Nrf2 signaling pathways under CNS demyelination, highlighting the importance of the antioxidant cellular response of neurodegenerative diseases such as MS.
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Registered trials
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