ArticleLife science alliance2019
MITOL deletion in the brain impairs mitochondrial structure and ER tethering leading to oxidative stress.
Article in Life science alliance, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 34 citations in OpenAlex.
- Mitochondria-ER contacts function as an iron supply hub.Nature cell biology · 2026Article
- Article
- Mitochondria and Endoplasmic Reticulum Contact Site as a Regulator of Proteostatic Stress Responses in Neurodegenerative Diseases.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025Review
- Outer mitochondrial membrane E3 Ub ligase MARCH5 controls de novo peroxisome biogenesis.Developmental cell · 2025Article
- MARCH5 promotes STING pathway activation by suppressing polymer formation of oxidized STING.EMBO reports · 2023Article
- Longitudinal in vivo metabolic labeling reveals tissue-specific mitochondrial proteome turnover rates and proteins selectively altered by parkin deficiency.Scientific reports · 2023Article
- Phospholipids alter activity and stability of mitochondrial membrane-bound ubiquitin ligase MARCH5.Life science alliance · 2022Article
- Nestin-dependent mitochondria-ER contacts define stem Leydig cell differentiation to attenuate male reproductive ageing.Nature communications · 2022Article
- Mitochondria-ER Tethering in Neurodegenerative Diseases.Cellular and molecular neurobiology · 2022Review
- Systems modeling predicts that mitochondria ER contact sites regulate the postsynaptic energy landscape.NPJ systems biology and applications · 2021Article
- ER-mitochondria contact sites in neurodegeneration: genetic screening approaches to investigate novel disease mechanisms.Cell death and differentiation · 2021Review
- Mitochondrial ubiquitin ligase alleviates Alzheimer's disease pathology via blocking the toxic amyloid-β oligomer generation.Communications biology · 2021Article
- Unraveling the Link Between Mitochondrial Dynamics and Neuroinflammation.Frontiers in immunology · 2021Review
- Endoplasmic Reticulum-Mitochondria Contact Sites-Emerging Intracellular Signaling Hubs.Frontiers in cell and developmental biology · 2021Review
- Overview of Mitochondrial E3 Ubiquitin Ligase MITOL/MARCH5 from Molecular Mechanisms to Diseases.International journal of molecular sciences · 2020Review
- Regulation of Mitochondrial ATP Production: CaTrends in molecular medicine · 2020Review
- Mitochondria-Associated Endoplasmic Reticulum Membranes (MAMs) and Their Prospective Roles in Kidney Disease.Oxidative medicine and cellular longevity · 2020Review
- MERCs. The Novel Assistant to Neurotransmission?Frontiers in neuroscience · 2020Review
- The Molecular Determinants of Mitochondrial Membrane Contact With ER, Lysosomes and Peroxisomes in Neuronal Physiology and Pathology.Frontiers in cellular neuroscience · 2020Article
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial abnormalities are associated with developmental disorders, although a causal relationship remains largely unknown. Here, we report that increased oxidative stress in neurons by deletion of mitochondrial ubiquitin ligase MITOL causes a potential neuroinflammation including aberrant astrogliosis and microglial activation, indicating that mitochondrial abnormalities might confer a risk for inflammatory diseases in brain such as psychiatric disorders. A role of MITOL in both mitochondrial dynamics and ER-mitochondria tethering prompted us to characterize three-dimensional structures of mitochondria in vivo. In MITOL-deficient neurons, we observed a significant reduction in the ER-mitochondria contact sites, which might lead to perturbation of phospholipids transfer, consequently reduce cardiolipin biogenesis. We also found that branched large mitochondria disappeared by deletion of MITOL. These morphological abnormalities of mitochondria resulted in enhanced oxidative stress in brain, which led to astrogliosis and microglial activation partly causing abnormal behavior. In conclusion, the reduced ER-mitochondria tethering and excessive mitochondrial fission may trigger neuroinflammation through oxidative stress.
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