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REVIEW article
Front. Immunol.
Sec. Inflammation
Volume 16 - 2025 | doi: 10.3389/fimmu.2025.1555910
This article is part of the Research Topic Neuroinflammation: Mechanisms and Therapeutic Interventions View all 6 articles
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Hypobaric hypoxia is widely recognized as a prominent risk factor for highaltitude cerebral edema (HACE), which contributes to the exacerbation of multiple pathological mechanisms, including oxidative stress, mitochondrial dysfunction, disruption of blood-brain barrier integrity, neuroinflammation, and neuronal apoptosis. Among these mechanisms, abnormalities in oxygen metabolism, including hypoxia, oxidative stress, and mitochondrial dysfunction, play pivotal roles in the pathophysiology of HACE. In this review, our objective is to enhance our comprehension of the underlying molecular mechanisms implicated in HACE by investigating the potential involvement of oxygen metabolism. Addressing aberrations in oxygen metabolism holds promise for providing innovative therapeutic strategies for managing HACE.
Keywords: oxygen metabolism, hypobaric hypoxia, Oxidative Stress, Mitochondrial dysfunction, High-altitude cerebral edema HACE, high-altitude cerebral edema, HH, hypobaric hypoxia, ATP, adenosine triphosphate, ROS, reactive oxygen species
Received: 05 Jan 2025; Accepted: 26 Feb 2025.
Copyright: © 2025 Li, Zhang, Zhang, Jin, Zheng, Mo and Da. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence:
Zejiao Da, Lanzhou University Second Hospital, Lanzhou, China
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