缺氧诱导因子-1α在高原低氧脑损伤中的研究进展*

陈敬威 杨 艺 魏艳娜 孙 娟 赵秀丽

解剖学杂志 ›› 2022, Vol. 45 ›› Issue (1) : 61-65.

解剖学杂志 ›› 2022, Vol. 45 ›› Issue (1) : 61-65. DOI: 10.3969/j.issn.1001-1633.2022.01.013
综述

缺氧诱导因子-1α在高原低氧脑损伤中的研究进展*

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Research progress of HIF-1α at hypoxic brain injury in high altitude*

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摘要

缺氧诱导因子-1(HIF-1)是一种调节人体对缺氧反应的关键因子。HIF-1α 是HIF-1 的活性亚基,为细胞 缺氧信号转导通路中的核心因子。缺氧条件下HIF-1α 显著增高,调控细胞增殖、凋亡、红细胞及血管生成等重 要过程。低压、低氧是高原环境的主要特点,近年来越来越多的平原居民前往高海拔地区工作、旅游,急进高原 暴露有发展成高原病的风险,发生脑损伤的风险明显增加。高原低氧所致脑损伤包括脑水肿、血脑屏障破坏、神 经细胞形态学改变等,其机制包括氧化应激、炎症反应、凋亡等,而HIF-1α 在调节上述过程中发挥着重要作用。 现就HIF-1α 在高原低氧脑损伤中的作用机制进行简要综述。

Abstract

Hypoxia inducible factor-1 (HIF-1) is a key factor which regulates the body response to hypoxia. HIF-1α is the active subunit of HIF-1, which is a core factor in the signal transduction pathway of cell hypoxia. The expression of HIF-1α is significantly increased in hypoxic conditions. HIF-1α is involved in the regulation of cell proliferation, apoptosis, erythropoiesis, angiogenesis and some other important processes. Low pressure and oxygen are the main characteristics of the plateau environment. In recent years, more and more plains people go to high-altitude areas for work and travel. Rapid exposure to the plateau could be developed to altitude sickness, and the risk of brain injury could also be increased. Brain damage caused by high altitude hypoxia includes brain edema, blood-brain barrier destruction, neuronal morphological changes and so on. The mechanisms include oxidative stress, inflammation, apoptosis and so on. HIF-1α plays an important role in regulating those process. This article briefly reviews the mechanism of HIF-1α at hypoxic brain injury in high altitude.

关键词

缺氧诱导因子-1α / 高原低氧 / 脑损伤

Key words

hypoxia inducible factor-1α / high altitude hypoxia / brain injury

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陈敬威 杨 艺 魏艳娜 孙 娟 赵秀丽. 缺氧诱导因子-1α在高原低氧脑损伤中的研究进展*[J]. 解剖学杂志, 2022, 45(1): 61-65 https://doi.org/10.3969/j.issn.1001-1633.2022.01.013
Research progress of HIF-1α at hypoxic brain injury in high altitude*[J]. Chinese Journal of Anatomy, 2022, 45(1): 61-65 https://doi.org/10.3969/j.issn.1001-1633.2022.01.013

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