ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2017
Mitochondrial DNA Double-Strand Breaks in Oligodendrocytes Cause Demyelination, Axonal Injury, and CNS Inflammation.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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The trial behind it
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Who cites it
34 citing papers in PubMed, 52 citations in OpenAlex.
- Distinct age-related pattern of mitochondrial somatic mutations across multiple sclerosis phenotypes.Journal of neurology · 2026Article
- Mitochondrial Network Dynamics in Aging: Cellular Mechanisms, Intercellular Communication, and Their Impact on Tissue Adaptability.International journal of molecular sciences · 2026Review
- Dying oligodendrocytes persist without mitochondria.bioRxiv : the preprint server for biology · 2026Article
- Unlocking extracellular mitochondria from bench to clinical application in stroke.Stem cells translational medicine · 2025Review
- Microglia-Derived Extracellular Vesicles Enhance Oligodendrocyte Maturation by Transcriptionally Regulating Mitochondrial Molecular Pathways.Cellular and molecular neurobiology · 2025Article
- Astroglial TNFR2 signaling regulates hippocampal synaptic function and plasticity in a sex dependent manner.Brain, behavior, and immunity · 2025Article
- Del Río Hortega's insights into oligodendrocytes: recent advances in subtype characterization and functional roles in axonal support and disease.Frontiers in neuroanatomy · 2025Review
- Factors influencing brain recovery from stroke via possible epigenetic changes.Future science OA · 2024Review
- Should We Consider Neurodegeneration by Itself or in a Triangulation with Neuroinflammation and Demyelination? The Example of Multiple Sclerosis and Beyond.International journal of molecular sciences · 2024Review
- Panobinostat Attenuates Experimental Autoimmune Encephalomyelitis in Mice via Suppressing Oxidative Stress-Related Neuroinflammation and Mitochondrial Dysfunction.International journal of molecular sciences · 2024Article
- Loss of the DNA repair protein, polynucleotide kinase/phosphatase, activates the type 1 interferon response independent of ionizing radiation.Nucleic acids research · 2024Article
- Axonal Regeneration after Spinal Cord Injury: Molecular Mechanisms, Regulatory Pathways, and Novel Strategies.Biology · 2024Review
- Mitochondrial dysfunction in chronic neuroinflammatory diseases (Review).International journal of molecular medicine · 2024Review
- Mitochondrial Dysfunction: A Key Player in Brain Aging and Diseases.Current issues in molecular biology · 2024Review
- Mechanisms Governing Oligodendrocyte Viability in Multiple Sclerosis and Its Animal Models.Cells · 2024Review
- O-GlcNAcylation is essential for therapeutic mitochondrial transplantation.Communications medicine · 2023Article
- Cell-Type-Specific Mitochondrial Quality Control in the Brain: A Plausible Mechanism of Neurodegeneration.International journal of molecular sciences · 2023Review
- The complexities of investigating mitochondria dynamics in multiple sclerosis and mouse models of MS.Frontiers in neuroscience · 2023Review
- Emerging role of STING signalling in CNS injury: inflammation, autophagy, necroptosis, ferroptosis and pyroptosis.Journal of neuroinflammation · 2022Review
- Cross-Talk between Amyloid, Tau Protein and Free Radicals in Post-Ischemic Brain Neurodegeneration in the Form of Alzheimer's Disease Proteinopathy.Antioxidants (Basel, Switzerland) · 2022Review
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 3 countries.
Funding
Abstract
Mitochondrial dysfunction has been implicated in the pathophysiology of neurodegenerative disorders, including multiple sclerosis (MS). To date, the investigation of mitochondrial dysfunction in MS has focused exclusively on neurons, with no studies exploring whether dysregulation of mitochondrial bioenergetics and/or genetics in oligodendrocytes might be associated with the etiopathogenesis of MS and other demyelinating syndromes. To address this question, we established a mouse model where mitochondrial DNA (mtDNA) double-strand breaks (DSBs) were specifically induced in myelinating oligodendrocytes (PLP:mtPstI mice) by expressing a mitochondrial-targeted endonuclease, mtPstI, starting at 3 weeks of age. In both female and male mice, DSBs of oligodendroglial mtDNA caused impairment of locomotor function, chronic demyelination, glial activation, and axonal degeneration, which became more severe with time of induction. In addition, after short transient induction of mtDNA DSBs, PLP:mtPstI mice showed an exacerbated response to experimental autoimmune encephalomyelitis. Together, our data demonstrate that mtDNA damage can cause primary oligodendropathy, which in turn triggers demyelination, proving PLP:mtPstI mice to be a useful tool to study the pathological consequences of mitochondrial dysfunction in oligodendrocytes. In addition, the demyelination and axonal loss displayed by PLP:mtPstI mice recapitulate some of the key features of chronic demyelinating syndromes, including progressive MS forms, which are not accurately reproduced in the models currently available. For this reason, the PLP:mtPstI mouse represents a unique and much needed platform for testing remyelinating therapies.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.