ArticleFrontiers in molecular neuroscience2023
High-altitude cerebral hypoxia promotes mitochondrial dysfunction and apoptosis of mouse neurons.
Article in Frontiers in molecular neuroscience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 15 citations in OpenAlex.
- Chronic high-altitude exposure and intracerebral hemorrhage: A novel perspective from the vascular-immune-neuronal network.Neuroprotection (Chichester, England) · 2026Review
- Altitude-Related Adaptation in Freshwater Snails (Animals : an open access journal from MDPI · 2026Article
- High-Altitude Hypoxia Activates JNK-p53 Signaling: Linking Hippocampal Energy Crisis to Cognitive Impairment.CNS neuroscience & therapeutics · 2026Article
- Olink Proteomics Reveals CCL2 Aggravates Perihematomal Edema After Intracerebral Hemorrhage in High-Altitude Migrants Via CCR2/NF-κB-Mediated Blood-Brain Barrier Disruption.CNS neuroscience & therapeutics · 2026Article
- Chronic hypoxia reshapes the brain: subregional volume reductions of the hippocampus and amygdala contrasts with behavioral resilience in long-term high-altitude migrants.Frontiers in neuroscience · 2026Article
- PANoptosis and mitochondrial regulatory mechanisms in cerebral ischemia-reperfusion injury.Frontiers in physiology · 2026Review
- Impact of Exposure Duration to High-Altitude Hypoxia on Oxidative Homeostasis in Rat Brain Regions.International journal of molecular sciences · 2025Article
- Trans-Sodium Crocetinate Ameliorates High-Altitude Acute Lung Injury via Modulating EGFR/PI3K/AKT/NF-κB Signaling Axis.Nutrients · 2025Article
- Mild hypothermia effects on serum neuroprotection, nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), and superoxide dismutase (SOD) levels in neonates with hypoxic-ischemic encephalopathy.Journal of medical biochemistry · 2025Article
- Limited Changes in Red Blood Cell Parameters After Probiotic Supplementation in Depressive Individuals: Insights from a Secondary Analysis of the PRO-DEMET Randomized Controlled Trial.Journal of clinical medicine · 2025Article
- Unraveling the complexity of cognitive impairment following high-altitude exposure: from preclinical animal models to human organoids.Frontiers in neuroscience · 2025Review
- Oxygen metabolism abnormalities and high-altitude cerebral edema.Frontiers in immunology · 2025Review
- Research Progress on Using Nanoparticles to Enhance the Efficacy of Drug Therapy for Chronic Mountain Sickness.Pharmaceutics · 2024Review
- High-altitude exposure and ischemic stroke: pathophysiological mechanisms and current perspectives.Frontiers in neurologyReview
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Neuronal cell death is an important factor in the pathogenesis of acute high-altitude cerebral hypoxia; however, the underlying molecular mechanism remains unclear. In this study, we tested if high-altitude hypoxia (HAH) causes neuronal death and mitochondrial dysfunction using various Methods: Acute high-altitude cerebral hypoxia was induced by hypobaric hypoxia chamber in male mice. we explored the mechanisms of neuronal cell death using immunofluorescence, western blotting, transmission electron microscopy, and flow cytometry. Next, mitochondrial function and morphology were observed using Jc-1 staining, seahorse assay, western blotting, MitoTracker staining, and transmission electron microscopy. Moreover, open field test, elevated plus test, and Morris water maze were applied for animal behavior. Results: Results revealed that HAH disrupted mitochondrial function and promoted neuronal apoptosis and necroptosis both in HT-22 cells and in mouse hippocampal neurons. Moreover, the mitochondrial membrane potential and adenosine triphosphate production decreased in neurons after HAH, while oxidative stress and mitochondrial fission increased. Behavioral studies suggested that HAH induced anxiety-like behavior and impaired spatial memory, while it had no effect on athletic ability. Discussion: These findings demonstrated that HAH promotes mitochondrial dysfunction and apoptosis of mouse neurons, thus providing new insights into the role of mitochondrial function and neuronal cell death in acute high-altitude cerebral hypoxia.
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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.