ArticleBrain pathology (Zurich, Switzerland)2023
Mic60 is essential to maintain mitochondrial integrity and to prevent encephalomyopathy.
Article in Brain pathology (Zurich, Switzerland), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 10 citations in OpenAlex.
- Neuronal YTHDF2 suppresses innate immune activation in Aβ pathology by promoting mScience advances · 2026Article
- Effects of an indole chemical, mitochonic acid 5, in a mouse model of mitochondrial disease onset.Scientific reports · 2026Article
- Early Reduction in Mitochondrial Membrane Potential in Synaptic Mitochondria Contribute to Synaptic Pathology in the EAE Mouse Model of Multiple Sclerosis.International journal of molecular sciences · 2026Article
- Mitophagy Activation by N-Acetylcysteine Protects against Mic60 Deficiency-Induced Auditory Neuropathy.Neuroscience bulletin · 2026Article
- PP2Acα regulates cerebellar development via phosphorylation-dependent neuronal programs.iScience · 2026Article
- Molecular Insights into Central Core Disease: Proteomic Signatures and Potential Therapeutic Biomarkers in RYR1 I4895T Mice.International journal of molecular sciences · 2025Article
- Structures and functions of the MICOS: Pathogenesis and therapeutic implications in Alzheimer's disease.Acta pharmaceutica Sinica. B · 2025Review
- Evaluating the mitochondrial structure and gene expression profile of regenerated liver tissues in mice after 85% partial hepatectomy.Journal of gastrointestinal oncology · 2024Article
- Mic60 is essential to maintain mitochondrial integrity and to prevent encephalomyopathy.Brain pathology (Zurich, Switzerland) · 2023Article
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Authors and funding
16 authors at 3 institutions in 1 country.
Funding
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Abstract
Mitochondrial encephalomyopathies (ME) are frequently associated with mutations of mitochondrial DNA, but the pathogenesis of a subset of ME (sME) remains elusive. Here we report that haploinsufficiency of a mitochondrial inner membrane protein, Mic60, causes progressive neurological abnormalities with insulted mitochondrial structure and neuronal loss in mice. In addition, haploinsufficiency of Mic60 reduces mitochondrial membrane potential and cellular ATP production, increases reactive oxygen species, and alters mitochondrial oxidative phosphorylation complexes in neurons in an age-dependent manner. Moreover, haploinsufficiency of Mic60 compromises brain glucose intake and oxygen consumption in mice, resembling human ME syndrome. We further discover that MIC60 protein expression declined significantly in human sME, implying that insufficient MIC60 may contribute for pathogenesis of human ME. Notably, systemic administration of antioxidant N-acetylcysteine largely reverses mitochondrial dysfunctions and metabolic disorders in haplo-insufficient Mic60 mice, also restores neurological abnormal symptom. These results reveal Mic60 is required in the maintenance of mitochondrial integrity and function, and likely a potential therapeutics target for mitochondrial encephalomyopathies.
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