线粒体功能障碍及线粒体DNA释放在脓毒症相关性急性肺损伤中作用的研究进展

Research advance on the role of mitochondrial dysfunction and releasing mitochondrial DNA in sepsis-induced acute lung injury

脓毒症相关性急性肺损伤(ALI)发生率较高,线粒体功能障碍及线粒体DNA(mtDNA)释放在脓毒症相关性ALI发生发展过程中具有至关重要的作用。脓毒症时线粒体功能障碍引起细胞能量耗竭和组织细胞修复机制障碍,导致ALI;此外,脓毒症时mtDNA释放可引起更强烈的炎症反应,加重脓毒症相关性ALI。本文通过对脓毒症时线粒体功能障碍和mtDNA释放的病理生理机制及相关研究现状进行综述,以期为脓毒症相关性ALI的病情评价、治疗和预防提供方向。

Sepsis-induced acute lung injury(ALI)is a serious condition with a high incidence.Mitochondrial dysfunction and the release of mitochondrial DNA(mtDNA)play a crucial role in the occurrence and development of sepsis-induced ALI.In sepsis,mitochondrial dysfunction causes energy depletion of cells and dysfunction of tissue cell repair mechanisms,leading to ALI.In addition,the release of mtDNA leads to a more intense inflammatory response,exacerbating sepsis-induced ALI.This article reviews the pathophysiological mechanism of mitochondrial dysfunction and mtDNA release in sepsis and the current research status,in order to provide direction for the evaluation,treatment and prevention of sepsis-induced ALI.