失血性休克导致器官功能障碍的新研究方向——线粒体质量控制机制

New research direction of organ dysfunction caused by hemorrhagic shock:mechanisms of mitochondrial quality control

失血性休克(HS)是全球青壮年人群的主要死亡原因之一。HS导致多器官功能障碍是由组织氧供需不平衡引起,与患者的不良预后密切相关。线粒体功能障碍是HS导致多器官功能障碍的重要机制之一,而线粒体质量控制可通过线粒体生物发生、线粒体动力学、线粒体自噬、线粒体衍生囊泡和线粒体蛋白稳态等一系列过程调控线粒体功能,调控线粒体质量控制可以改善器官功能障碍。本文就线粒体功能障碍对HS器官功能的影响及线粒体质量控制的可能机制进行综述,以期进一步了解HS的损伤机制并指导临床救治。

Hemorrhagic shock(HS)is one of the leading causes of death among young adults worldwide.Multiple organ dysfunction in HS is caused by an imbalance between tissue oxygen supply and demand,which is closely related to the poor prognosis of patient.Mitochondrial dysfunction is one of the key mechanisms contributing to multiple organ dysfunction in HS,while mitochondrial quality control regulates mitochondrial function through a series of processes,including mitochondrial biogenesis,mitochondrial dynamics,mitophagy,mitochondrial-derived vesicles,and mitochondrial protein homeostasis.Modulating mitochondrial quality control can improve organ dysfunction.This review aims to summarize the effects of mitochondrial dysfunction on organ function in HS and discuss the potential mechanisms of mitochondrial quality control,providing insights into the injury mechanisms underlying HS and guiding clinical management.