ArticleGlia2010
Injury and differentiation following inhibition of mitochondrial respiratory chain complex IV in rat oligodendrocytes.
Article in Glia, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 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.
The trial behind it
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
59 citing papers in PubMed, 102 citations in OpenAlex.
- Is there a link between multiple sclerosis and Alzheimer disease? A critical note.Journal of neural transmission (Vienna, Austria : 1996) · 2026Review
- N-Acetylglucosamine Selectively Attenuates Neuroinflammation in a Mouse Model of Mitochondrial Dysfunction.Acta physiologica (Oxford, England) · 2026Article
- A Human Model of Oligodendrocyte Development Shows MCL-1 Influences Oligodendrocyte Morphogenesis.Glia · 2026Article
- Dying oligodendrocytes persist without mitochondria.bioRxiv : the preprint server for biology · 2026Article
- Glial lactate metabolism and transport in Alzheimer's disease.Frontiers in aging neuroscience · 2026Review
- Metabolic Reprogramming of Oligodendrocytes in Intrauterine Growth Restriction.Developmental neuroscience · 2026Article
- Significant Suppression of Multiple Sclerosis in the Mouse EAE Model Using the PrC-210 Aminothiol.International journal of molecular sciences · 2025Article
- Review
- Blood-Based Lateral-Flow Immunoassays Dipstick Test for Damaged Mitochondrial Electron Transport Chain in Pyruvate Treated Rats with Combined Blast Exposure and Hemorrhagic Shock.Journal of clinical medicine · 2025Article
- The isoflavone puerarin promotes generation of human iPSC-derived pre-oligodendrocytes and enhances endogenous remyelination in rodent models.Journal of neurochemistry · 2025Article
- MCL-1 regulates cellular transitions during oligodendrocyte development.bioRxiv : the preprint server for biology · 2024Article
- Pyruvate Dehydrogenase-Dependent Metabolic Programming Affects the Oligodendrocyte Maturation and Remyelination.Molecular neurobiology · 2024Article
- FKBP5 activates mitophagy by ablating PPAR-γ to shape a benign remyelination environment.Cell death & disease · 2023Article
- Smouldering Lesion in MS: Microglia, Lymphocytes and Pathobiochemical Mechanisms.International journal of molecular sciences · 2023Review
- Emerging mitochondrial-mediated mechanisms involved in oligodendrocyte development.Journal of neuroscience research · 2023Review
- Exploring Shared Genetic Signatures of Alzheimer's Disease and Multiple Sclerosis: A Bioinformatic Analysis Study.European neurology · 2023Article
- The AMPK activator metformin improves recovery from demyelination by shifting oligodendrocyte bioenergetics and accelerating OPC differentiation.Frontiers in cellular neuroscience · 2023Article
- Mitochondrial dysfunctions induce PANoptosis and ferroptosis in cerebral ischemia/reperfusion injury: from pathology to therapeutic potential.Frontiers in cellular neuroscience · 2023Review
- A case of primary optic pathway demyelination caused by oncocytic oligodendrogliopathy of unknown origin.Acta neuropathologica communications · 2022Article
- The contribution of neuropathology to multiple sclerosis research.European journal of neurology · 2022Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Oligodendrocyte lineage cells are susceptible to a variety of insults including hypoxia, excitotoxicity, and reactive oxygen species. Demyelination is a well-recognized feature of several CNS disorders including multiple sclerosis, white matter strokes, progressive multifocal leukoencephalopathy, and disorders due to mitochondrial DNA mutations. Although mitochondria have been implicated in the demise of oligodendrocyte lineage cells, the consequences of mitochondrial respiratory chain defects have not been examined. We determine the in vitro impact of established inhibitors of mitochondrial respiratory chain complex IV or cytochrome c oxidase on oligodendrocyte progenitor cells (OPCs) and mature oligodendrocytes as well as on differentiation capacity of OPCs from P0 rat. Injury to mature oligodendrocytes following complex IV inhibition was significantly greater than to OPCs, judged by cell detachment and mitochondrial membrane potential (MMP) changes, although viability of cells that remained attached was not compromised. Active mitochondria were abundant in processes of differentiated oligodendrocytes and MMP was significantly greater in differentiated oligodendrocytes than OPCs. MMP dissipated following complex IV inhibition in oligodendrocytes. Furthermore, complex IV inhibition impaired process formation within oligodendrocyte lineage cells. Injury to and impaired process formation of oligodendrocytes following complex IV inhibition has potentially important implications for the pathogenesis and repair of CNS myelin disorders.
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What OpenQuestion holds
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.