Zhi Li, Jianping Zhang, Xiaoxia Zhang, Qiaoying Jin, Xingxing Zheng, Li Mo, Zejiao Da
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引用次数: 0
Abstract
Hypobaric hypoxia is widely recognized as a prominent risk factor for high-altitude 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.
期刊介绍:
Frontiers in Immunology is a leading journal in its field, publishing rigorously peer-reviewed research across basic, translational and clinical immunology. This multidisciplinary open-access journal is at the forefront of disseminating and communicating scientific knowledge and impactful discoveries to researchers, academics, clinicians and the public worldwide.
Frontiers in Immunology is the official Journal of the International Union of Immunological Societies (IUIS). Encompassing the entire field of Immunology, this journal welcomes papers that investigate basic mechanisms of immune system development and function, with a particular emphasis given to the description of the clinical and immunological phenotype of human immune disorders, and on the definition of their molecular basis.