ArticleNeurocritical care2020
Extracellular Mitochondrial Dysfunction in Cerebrospinal Fluid of Patients with Delayed Cerebral Ischemia after Aneurysmal Subarachnoid Hemorrhage.
Article in Neurocritical care, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 35 citations in OpenAlex.
- Intercellular Mitochondrial Transfer as Endogenous Neuroprotection: Mechanisms and Therapeutic Implications in Ischemic Stroke.Translational stroke research · 2026Review
- Brain-targeted extracellular vesicles for anti-cuproptosis therapy in subarachnoid haemorrhage.Stroke and vascular neurology · 2026Article
- Unlocking extracellular mitochondria from bench to clinical application in stroke.Stem cells translational medicine · 2025Review
- Astrocyte-microglia crosstalk in subarachnoid hemorrhage: mechanisms and treatments.Frontiers in immunology · 2025Review
- Mitochondrial dysfunction and quality control lie at the heart of subarachnoid hemorrhage.Neural regeneration research · 2024Review
- Autophagy and mitophagy-related extracellular mitochondrial dysfunction of cerebrospinal fluid cells in patients with hemorrhagic moyamoya disease.Scientific reports · 2023Article
- Biomarkers in aneurysmal subarachnoid hemorrhage: A short review.World neurosurgery: X · 2023Review
- The Critical Role of Sirt1 in Subarachnoid Hemorrhages: Mechanism and Therapeutic Considerations.Brain sciences · 2023Review
- Bioinformatics Analysis of Autophagy and Mitophagy Markers Associated with Delayed Cerebral Ischemia Following Subarachnoid Hemorrhage.Journal of Korean Neurosurgical Society · 2022Article
- New Mechanisms and Targets of Subarachnoid Hemorrhage: A Focus on Mitochondria.Current neuropharmacology · 2022Review
- Mitochondrial dysfunction associated with autophagy and mitophagy in cerebrospinal fluid cells of patients with delayed cerebral ischemia following subarachnoid hemorrhage.Scientific reports · 2021Article
- Profiling of T Cell Receptor β-Chain Complimentary Determining Regions 3 Repertoire in Subarachnoid Hemorrhage Patients Using High-Throughput Sequencing.Journal of Korean Neurosurgical Society · 2021Article
- Neuroprotective Strategies in Aneurysmal Subarachnoid Hemorrhage (aSAH).International journal of molecular sciences · 2021Review
- Extracellular Mitochondria Signals in CNS Disorders.Frontiers in cell and developmental biology · 2021Review
- Inflammation and Oxidative Stress: Potential Targets for Improving Prognosis After Subarachnoid Hemorrhage.Frontiers in cellular neuroscience · 2021Review
- Characterization of the TCR β Chain CDR3 Repertoire in Subarachnoid Hemorrhage Patients with Delayed Cerebral Ischemia.International journal of molecular sciences · 2020Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMitochondrial dysfunction is related to brain ischemic injury and neural cell death. However, little is known about the association between mitochondrial dysfunction of cerebrospinal fluid (CSF) and delayed cerebral ischemia (DCI) following subarachnoid hemorrhage (SAH). The objective of this study was to investigate whether extracellular CSF mitochondria might serve as a potential biomarker for DCI.
methodsCSF samples were serially collected at 1, 3, and 5 days following SAH in 33 patients (DCI, n = 12; and non-DCI, n = 21) who underwent coil embolization. To monitor mitochondrial membrane potentials, JC-1 dye was used. The ratio (red/green) of JC-1 was considered as an indicator of intact mitochondrial membrane potential. Flow cytometry was done to analyze extracellular mitochondria particles and their possible cellular origins.
resultsDCI patients had lower JC-1 red/green ratios than non-DCI patients at 1 day (3.35 [3.20-3.75] vs. 3.70 [3.40-3.95] in non-DCI) and 3 days (4.65 [4.45-5.00] vs. 5.10 [4.65-5.30] in non-DCI) after SAH. At 5 days after SAH, JC-1 red/green ratio was significantly lower in DCI than that in non-DCI (3.05 [2.90-3.35] vs. 4.20 [4.10-4.50]; p < 0.01) patients. DCI patients had a higher percentage of vWF-positive mitochondria (40.10% [38.25%-44.90%] vs. 30.20% [25.70%-36.68%]) and a lower percentage of GLAST-positive mitochondria particles (26.85% [17.10%-30.00%] vs. 31.60% [26.70%-35.00%]) than non-DCI patients. However, there was no significant difference in CD45-positive (p = 0.369) or CD41/61-positive mitochondrial particles (p = 0.155) between the two groups of patients.
conclusionsMitochondrial membrane potential could be a marker of DCI. JC-1 ratios seemed to be able to predict future DCI onset. Further studies are needed to determine detailed mechanisms of extracellular mitochondria-mediated cell-to-cell signals in DCI.
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