高原缺氧脑损伤分子机制的研究进展

Research Progress on Molecular Mechanism of High Altitude Hypoxic Brain Injury

随着高原旅游业的发展及西部大开发的推进,高原逐渐成为研究的热点问题。人体内对缺氧最敏感的脑组织在高原环境中会出现一系列生理病理改变,目前高原缺氧脑损伤的分子机制尚不明确,临床上亦缺少有效的预防治疗靶点及措施。本文分析总结了近五年国内外对高原缺氧脑损伤分子机制的研究,将从神经元线粒体自噬、细胞内钙超载、血脑屏障损伤、脑血流量的变化、炎症反应、认知功能受损等方面进行综述,希望为高原缺氧脑损伤的研究提供新的思路和方向。

With the development of plateau tourism and the promotion of western development,plateau has gradually become a hot issue of research.A series of physiological and pathological changes may occur in the brain tissues most sensitive to hypoxia in human body in the altitude environment.At present,the molecular mechanism of brain injury caused by altitude hypoxia is not clear,and effective prevention treatment targets and measures are lacking in clinic.This article analyzes and summarizes the research on the molecular mechanism of high altitude hypoxic brain injury in the past five years at home and abroad.It will review the aspects of neuronal mitochondrial autophagy,intracellular calcium overload,blood-brain barrier damage,changes in cerebral blood flow,inflammatory response,cognitive impairment,etc,which hopes to provide new ideas and directions for the study of high altitude hypoxic brain injury.