ArticleFrontiers in molecular neuroscience2017
Loss of Mitochondrial
Article in Frontiers in molecular neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
12 citing papers in PubMed, 20 citations in OpenAlex.
- Mitochondrial complex I deficiency-associated diseases and models.Cellular and molecular life sciences : CMLS · 2026Review
- Epigenome-wide association study of nuclear DNA methylation in relation to mitochondrial heteroplasmy.Nature communications · 2025Article
- Disease models of Leigh syndrome: From yeast to organoids.Journal of inherited metabolic disease · 2024Review
- Differential timing of mitochondrial activation in rat dorsal striatum induced by procedural learning and swimming.Frontiers in molecular neuroscience · 2024Article
- Neurological Phenotypes in Mouse Models of Mitochondrial Disease and Relevance to Human Neuropathology.International journal of molecular sciences · 2023Review
- Ndufs4 knockout mouse models of Leigh syndrome: pathophysiology and intervention.Brain : a journal of neurology · 2022Review
- Natural History of Leigh Syndrome: A Study of Disease Burden and Progression.Annals of neurology · 2022Observational
- Ndufs4 ablation decreases synaptophysin expression in hippocampus.Scientific reports · 2021Article
- Myopathy reversion in mice after restauration of mitochondrial complex I.EMBO molecular medicine · 2020Article
- Mitochondrial Proteome of Affected Glutamatergic Neurons in a Mouse Model of Leigh Syndrome.Frontiers in cell and developmental biology · 2020Article
- Article
- FOXRED1 silencing in mice: a possible animal model for Leigh syndrome.Metabolic brain disease · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Inability of mitochondria to generate energy leads to severe and often fatal myoencephalopathies. Among these, Leigh syndrome (LS) is one of the most common childhood mitochondrial diseases; it is characterized by hypotonia, failure to thrive, respiratory insufficiency and progressive mental and motor dysfunction, leading to early death. Basal ganglia nuclei, including the striatum, are affected in LS patients. However, neither the identity of the affected cell types in the striatum nor their contribution to the disease has been established. Here, we used a mouse model of LS lacking
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Registered trials
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