摘要
失血性休克(HS)是指大量出血导致有效循环血容量急剧减少,组织灌注不足而引起的一种急性循环衰竭状态。HS易引发一系列复杂病理生理变化,其中线粒体功能障碍被视为关键环节。线粒体是细胞能量生产中心,参与调节细胞凋亡、氧化应激反应及免疫调控等多方面生物学过程,HS状态下,线粒体遭受损伤后影响自身功能,进一步加剧全身炎症反应、组织缺氧及多器官功能衰竭。近年来,随着对HS病理生理机制的深入研究,线粒体在其中扮演的角色越来越受到重视,然而其作用机制尚不明确。该文就HS后线粒体损伤的病理生理特征、分子调控机制及治疗药物进展进行综述,旨在为今后此方向的发展与完善提供有益参考。
Hemorrhagic shock(HS)is a state of acute circulatory failure caused by massive hemorrhage that results in a sharp decrease in effective circulating blood volume and tissue hypoperfusion.HS easily triggers a series of complex pathophysiological changes,among which mitochondrial dysfunction is regarded as a key link.Mitochondria are the center of cellular energy production,which are involved in the regulation of apoptosis,oxidative stress response and immune regulation.With in-depth studies on the pathophysiological mechanism of HS,the role of mitochondria in HS has received more attention,but the mechanism of action remains elusive.This article reviews the pathophysiological characteristics,molecular regulatory mechanisms and research progress related to therapeutic drugs for mitochondrial injury after HS in order to contribute to subsequent research in this area.
作者
李俊英
刘磊
LI Junying;LIU Lei(Medical College,Wuhan University of Science and Technology,Wuhan 430065,China;Department of Transfusion Medicine,General Hospital of Central Theater Command,Wuhan 430070,China)
出处
《军事医学》
2025年第11期864-869,共6页
Military Medical Sciences
基金
湖北省医学青年拔尖人才项目[鄂卫通(2023)65号]。
关键词
失血性休克
线粒体损伤
氧化应激
沉默信息调节因子1
线粒体保护剂
hemorrhagic shock
mitochondrial injury
oxidative stress
silent information regulation 1
mitochondrial protectants
