ArticleMolecular neurobiology2021
Metallothionein 1 Overexpression Does Not Protect Against Mitochondrial Disease Pathology in Ndufs4 Knockout Mice.
Article in Molecular neurobiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Tissue-Specific Regulation of Fatty Acid Metabolism in a Mouse Model of Isolated Complex I Deficiency.Proteomics · 2025Article
- Hepatic bioenergetics and metabolism in mitochondrial disease: insights from the Ndufs4 KO mouse model.Metabolomics : Official journal of the Metabolomic Society · 2025Article
- Cannabidiol ameliorates mitochondrial disease via PPARγ activation in preclinical models.Nature communications · 2024Article
- Microglial response promotes neurodegeneration in the Ndufs4 KO mouse model of Leigh syndrome.Glia · 2022Article
- Ndufs4 knockout mouse models of Leigh syndrome: pathophysiology and intervention.Brain : a journal of neurology · 2022Review
- On the dynamic and even reversible nature of Leigh syndrome: Lessons from human imaging and mouse models.Current opinion in neurobiology · 2022Review
- Cross-comparison of systemic and tissue-specific metabolomes in a mouse model of Leigh syndrome.Metabolomics : Official journal of the Metabolomic Society · 2021Article
- Sub-Cellular Metabolomics Contributes Mitochondria-Specific Metabolic Insights to a Mouse Model of Leigh Syndrome.Metabolites · 2021Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
Abstract
Mitochondrial diseases (MD), such as Leigh syndrome (LS), present with severe neurological and muscular phenotypes in patients, but have no known cure and limited treatment options. Based on their neuroprotective effects against other neurodegenerative diseases in vivo and their positive impact as an antioxidant against complex I deficiency in vitro, we investigated the potential protective effect of metallothioneins (MTs) in an Ndufs4 knockout mouse model (with a very similar phenotype to LS) crossed with an Mt1 overexpressing mouse model (TgMt1). Despite subtle reductions in the expression of neuroinflammatory markers GFAP and IBA1 in the vestibular nucleus and hippocampus, we found no improvement in survival, growth, locomotor activity, balance, or motor coordination in the Mt1 overexpressing Ndufs4
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Registered trials
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