ArticleCNS neuroscience & therapeutics2019
Prophylactic treatment of hyperbaric oxygen treatment mitigates inflammatory response via mitochondria transfer.
Article in CNS neuroscience & therapeutics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 2 of them syntheses that pooled it.
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Who cites it
48 citing papers in PubMed, 2 syntheses or guidelines pooled it, 70 citations in OpenAlex.
- Mitochondria transfer research from cellular mechanisms to immune-inflammatory and translational frontiers: a bibliometric analysis from 2006 to 2026.Frontiers in immunology · 2026Pooled it
- Mitochondrial Transfer in the Neurovascular Unit, Not Only for Energy Rescue: A Systematic Review.Aging and disease · 2024Pooled it
- Hyperbaric oxygen therapy: a novel treatment option in complex regional pain syndrome and other chronic pain conditions.Medical gas research · 2026Article
- Intercellular Mitochondrial Transfer as Endogenous Neuroprotection: Mechanisms and Therapeutic Implications in Ischemic Stroke.Translational stroke research · 2026Review
- Modeling CLN3 Batten disease in astrocytes reveals alterations in mitochondria homeostasis, fatty acid metabolism and oxidative stress response.Journal of biomedical science · 2026Article
- MitoTracker transfers from astrocytes to neurons independently of mitochondria.Cell reports methods · 2026Article
- Unlocking extracellular mitochondria from bench to clinical application in stroke.Stem cells translational medicine · 2025Review
- The Role of Astrocytes in Poststroke Rehabilitation.Brain and behavior · 2025Review
- Therapeutic implications of mitochondrial transfer on stem cell fate in regenerative medicine.Journal of translational medicine · 2025Review
- Effect of hyperbaric oxygen therapy on peripheral blood inflammatory markers in patients with neuromyelitis optica spectrum disorder: a retrospective cohort study.Frontiers in neurology · 2025Article
- Darbepoetin alpha has an anxiolytic and anti-neuroinflammatory effect in male rats.BMC immunology · 2024Article
- Mitochondrial Transportation, Transplantation, and Subsequent Immune Response in Alzheimer's Disease: An Update.Molecular neurobiology · 2024Review
- CD36 deletion prevents white matter injury by modulating microglia polarization through the Traf5-MAPK signal pathway.Journal of neuroinflammation · 2024Article
- Hyperbaric oxygen therapy as a neuromodulatory technique: a review of the recent evidence.Frontiers in neurology · 2024Review
- Hypoxic ischemic encephalopathy (HIE).Frontiers in neurology · 2024Review
- Mitochondrial dysfunction and Alzheimer's disease: pathogenesis of mitochondrial transfer.Frontiers in aging neuroscience · 2024Review
- 100% oxygen mobilizes stem cells and up-regulates MIF and APRIL in humans: a new point on the hormetic dose curve.Frontiers in cell and developmental biology · 2024Article
- Identifying the Target Traumatic Brain Injury Population for Hyperbaric Oxygen Therapy.International journal of molecular sciences · 2023Review
- Highly Specialized Mechanisms for Mitochondrial Transport in Neurons: From Intracellular Mobility to Intercellular Transfer of Mitochondria.Biomolecules · 2023Review
- Mitochondria on the move: Horizontal mitochondrial transfer in disease and health.The Journal of cell biology · 2023Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
aimsHyperbaric oxygen therapy (HBOT) has been widely used as postinjury treatment; however, we investigate its ability to mitigate potential damage as a preconditioning option. Here, we tested the hypothesis that HBOT preconditioning mitigates cell death in primary rat neuronal cells (PRNCs) through the transfer of mitochondria from astrocytes.
methodsPrimary rat neuronal cells were subjected to a 90-minute HBOT treatment at 2.5 absolute atmospheres prior to either tumor necrosis factor-alpha (TNF-alpha) or lipopolysaccharide (LPS) injury to simulate the inflammation-plagued secondary cell death associated with stroke and traumatic brain injury (TBI). After incubation with TNF-alpha or LPS, the cell viability of each group was examined.
resultsThere was a significant increase of cell viability accompanied by mitochondrial transfer in the injury groups that received HBOT preconditioning compared to the injury alone groups (44 ± 5.2 vs 68 ± 4.48, n = 20, P < 0.05). The transfer of mitochondria directly after HBOT treatment was visualized by capturing images in 5-minute intervals, which revealed that the robust transfer of mitochondria begins soon after HBOT and persisted throughout the treatment.
conclusionThis study shows that HBOT preconditioning stands as a robust prophylactic treatment for sequestration of inflammation inherent in stroke and TBI, possibly facilitating the transfer of resilient mitochondria from astrocytes to inflammation-susceptible neuronal cells in mitigating cell death.
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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.