ArticleConditioning medicine2018
Mitochondrial dynamics and preconditioning in white matter.
Article in Conditioning medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.
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
14 citing papers in PubMed, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.
- Associations of Mitochondrial Function, Stress, and Neurodevelopmental Outcomes in Early Life: A Systematic Review.Developmental neuroscience · 2022Pooled it
- Oxygen-Glucose Deprivation Decreases the Motility and Length of Axonal Mitochondria in Cultured Dorsal Root Ganglion Cells of Rats.Cellular and molecular neurobiology · 2023Article
- Commentary: Can astrocytic mitochondria therapy be used as antioxidant conditioning to protect neurons?Conditioning medicine · 2022Article
- Aging astrocytes metabolically support aging axon function by proficiently regulating astrocyte-neuron lactate shuttle.Experimental neurology · 2022Article
- The Alterations in Mitochondrial Dynamics Following Cerebral Ischemia/Reperfusion Injury.Antioxidants (Basel, Switzerland) · 2021Review
- Mitochondria as the memory of preconditioning.Conditioning medicine · 2021Article
- Ischemic Neuroprotectant PKCε Restores Mitochondrial Glutamate Oxaloacetate Transaminase in the Neuronal NADH Shuttle after Ischemic Injury.Translational stroke research · 2020Article
- RNA sequencing reveals novel macrophage transcriptome favoring neurovascular plasticity after ischemic stroke.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2020Article
- Ex Vivo Studies of Optic Nerve Axon Electrophysiology.Methods in molecular biology (Clifton, N.J.) · 2020Article
- Preserving Mitochondrial Structure and Motility Promotes Recovery of White Matter After Ischemia.Neuromolecular medicine · 2019Article
- Near infrared light amplifies endothelial progenitor cell accumulation after stroke.Conditioning medicine · 2019Article
- CK2 inhibition confers functional protection to young and aging axons against ischemia by differentially regulating the CDK5 and AKT signaling pathways.Neurobiology of disease · 2019Article
- CK2 inhibition protects white matter from ischemic injury.Neuroscience letters · 2018Review
- NOS3 Inhibition Confers Post-Ischemic Protection to Young and Aging White Matter Integrity by Conserving Mitochondrial Dynamics and Miro-2 Levels.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Mechanisms of ischemic preconditioning have been extensively studied in gray matter. However, an ischemic episode affects both the gray matter (GM) and white matter (WM) portions of the brain. Inhibition of mitochondrial fission is one of the mechanisms of preconditioning neuronal cell bodies against ischemia. Although axons are anatomical extensions of neuronal cell bodies, injury mechanisms differ between GM and WM. Indeed, axonal dysfunction is responsible for much of the disability associated with clinical deficits observed after stroke; however, the signaling process underlying preconditioning remains unexplored in axons. Using mouse optic nerve, which is a pure isolated WM tract, we show that mitochondria in myelinated axons undergo rapid and profuse fission during oxygen glucose deprivation (OGD) that is mediated by translocation of cytoplasmic Dynamin Related Protein-1 (Drp-1) to mitochondria. OGD-induced mitochondrial fission correlates with reduced mitochondrial motility and loss of axon function. Mitochondrial fragmentation and loss of motility become permanent during the recovery period. Inhibiting mitochondrial fission by administering mitochondrial division inhibitor-1 (Mdivi-1) during OGD preserves mitochondrial shape and motility and promotes axon function recovery. In contrast, preconditioning WM by applying Mdivi-1 only before OGD fails to conserve mitochondrial shape or motility and fails to benefit axon function. Our findings suggest that inhibition of mitochondrial fission during ischemia promotes axon function recovery, but is not sufficient to precondition WM against ischemia. These results raise caution in that approaches to preconditioning neuronal cell bodies may not successfully translate into functional improvement following ischemia.
Indexed as
Identifiers
30135960PMC6101249W2975200985What 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.