ArticleNeuroscience bulletin2024
Impairment of Autophagic Flux After Hypobaric Hypoxia Potentiates Oxidative Stress and Cognitive Function Disturbances in Mice.
Article in Neuroscience bulletin, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 5 citations in OpenAlex.
- Chronic high-altitude exposure and intracerebral hemorrhage: A novel perspective from the vascular-immune-neuronal network.Neuroprotection (Chichester, England) · 2026Review
- Article
- Microglial cholesterol reprogramming drives cognitive impairment under hypobaric hypoxia.Journal of neuroinflammation · 2026Article
- Hypoxic Preconditioning Mitigates Acute Hypoxia Induced MS/VDB Cholinergic Cell Loss and Memory Impairments.Aging and disease · 2025Article
- [Application of Animal Models in Research on Hypoxia-Related Diseases].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2025Review
- Tetramethylpyrazine exerts neuroprotective effects in a mouse model of acute hypobaric hypoxia.Frontiers in pharmacology · 2025Article
- Huangqi Baihe Granules Attenuate Hypobaric Hypoxia-Induced Brain Injury via HIF-1a/p53/Caspase-3 Pathway.Drug design, development and therapy · 2025Article
- Potential therapeutic effects of traditional Chinese medicine in acute mountain sickness: pathogenesis, mechanisms and future directions.Frontiers in pharmacology · 2024Review
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute hypobaric hypoxic brain damage is a potentially fatal high-altitude sickness. Autophagy plays a critical role in ischemic brain injury, but its role in hypobaric hypoxia (HH) remains unknown. Here we used an HH chamber to demonstrate that acute HH exposure impairs autophagic activity in both the early and late stages of the mouse brain, and is partially responsible for HH-induced oxidative stress, neuronal loss, and brain damage. The autophagic agonist rapamycin only promotes the initiation of autophagy. By proteome analysis, a screen showed that protein dynamin2 (DNM2) potentially regulates autophagic flux. Overexpression of DNM2 significantly increased the formation of autolysosomes, thus maintaining autophagic flux in combination with rapamycin. Furthermore, the enhancement of autophagic activity attenuated oxidative stress and neurological deficits after HH exposure. These results contribute to evidence supporting the conclusion that DNM2-mediated autophagic flux represents a new therapeutic target in HH-induced brain damage.
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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.