Dokumentdetails
ID
oai:pubmedcentral.nih.gov:1077...
Thema
Original ArticleAutor
Dai, Shuhui Feng, Yuan Lu, Chuanhao Zhang, Hongchen Ma, Wenke Xie, Wenyu Wu, Xiuquan Luo, Peng Zhang, Lei Fei, Fei Fei, Zhou Li, XiaLangue
enEditor
Springer Nature Singapore
Kategorie
Neuroscience Bulletin
Jahr
2023
Auflistungsdatum
17.01.2024
Schlüsselwörter
hypobaric stress oxidative damage flux autophagic brainZusammenfassung
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.
SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s12264-023-01099-6.
Dai, Shuhui,Feng, Yuan,Lu, Chuanhao,Zhang, Hongchen,Ma, Wenke,Xie, Wenyu,Wu, Xiuquan,Luo, Peng,Zhang, Lei,Fei, Fei,Fei, Zhou,Li, Xia, 2023, Impairment of Autophagic Flux After Hypobaric Hypoxia Potentiates Oxidative Stress and Cognitive Function Disturbances in Mice, Springer Nature Singapore
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