ArticleThe Journal of clinical investigation2020
Cyclophilin D-dependent oligodendrocyte mitochondrial ion leak contributes to neonatal white matter injury.
Article in The Journal of clinical investigation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 18 citations in OpenAlex.
- Brown fat protects against hepatic oxidative stress by remodeling the circulating metabolome.Cell metabolism · 2026Article
- Genetic Deletion of Cyclophilin D Results in Enhanced Hypoxia Tolerance in Mice.Cellular and molecular neurobiology · 2026Article
- Mitochondrial Dysfunction in Neurodegenerative Diseases: Mechanisms and Corresponding Therapeutic Strategies.Biomedicines · 2025Review
- Exosomal LncRNA TM7SF3-AU1 Aggravates White Matter Injury via MiR-702-3p/SARM1 Signaling After Subarachnoid Hemorrhage in Rats.Molecular neurobiology · 2024Article
- Identity, structure, and function of the mitochondrial permeability transition pore: controversies, consensus, recent advances, and future directions.Cell death and differentiation · 2023Review
- Both ANT and ATPase are essential for mitochondrial permeability transition but not depolarization.iScience · 2022Article
- Developmental window of vulnerability to white matter injury driven by sublethal intermittent hypoxemia.Pediatric research · 2022Article
- Mitochondria-Related Ferroptosis Drives Cognitive Deficits in Neonatal Mice Following Sevoflurane Administration.Frontiers in medicine · 2022Article
- Intermittent Hypoxia Rewires the Liver Transcriptome and Fires up Fatty Acids Usage for Mitochondrial Respiration.Frontiers in medicine · 2022Article
- Mitochondrial Dysfunction and Permeability Transition in Neonatal Brain and Lung Injuries.Cells · 2021Review
- Electrophysiological properties of the mitochondrial permeability transition pores: Channel diversity and disease implication.Biochimica et biophysica acta. Bioenergetics · 2021Review
- A Potential ceRNA Network for Neurological Damage in Preterm Infants.BioMed research international · 2021Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Postnatal failure of oligodendrocyte maturation has been proposed as a cellular mechanism of diffuse white matter injury (WMI) in premature infants. However, the molecular mechanisms for oligodendrocyte maturational failure remain unclear. In neonatal mice and cultured differentiating oligodendrocytes, sublethal intermittent hypoxic (IH) stress activated cyclophilin D-dependent mitochondrial proton leak and uncoupled mitochondrial respiration, leading to transient bioenergetic stress. This was associated with development of diffuse WMI: poor oligodendrocyte maturation, diffuse axonal hypomyelination, and permanent sensorimotor deficit. In normoxic mice and oligodendrocytes, exposure to a mitochondrial uncoupler recapitulated the phenotype of WMI, supporting the detrimental role of mitochondrial uncoupling in the pathogenesis of WMI. Compared with WT mice, cyclophilin D-knockout littermates did not develop bioenergetic stress in response to IH challenge and fully preserved oligodendrocyte maturation, axonal myelination, and neurofunction. Our study identified the cyclophilin D-dependent mitochondrial proton leak and uncoupling as a potentially novel subcellular mechanism for the maturational failure of oligodendrocytes and offers a potential therapeutic target for prevention of diffuse WMI in premature infants experiencing chronic IH stress.
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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.