Zhang Jiuzhi
Department of Critical Care Medicine, the First Affiliated Hospital of Dalian Medical University, Dalian 116021, Liaoning, China. Corresponding author: Zhang Jiuzhi, Email:
Zhonghua Wei Zhong Bing Ji Jiu Yi Xue. 2024 Jan;36(1):102-105. doi: 10.3760/cma.j.cn121430-20230828-00702.
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.
脓毒症诱导的急性肺损伤（ALI）是一种发病率很高的严重病症。线粒体功能障碍和线粒体DNA（mtDNA）的释放，在脓毒症诱导的ALI的发生和发展中起着关键作用。在脓毒症中，线粒体功能障碍导致细胞能量耗竭和组织细胞修复机制功能障碍，进而引发ALI。此外，mtDNA的释放会导致更强烈的炎症反应，加剧脓毒症诱导的ALI。本文综述了脓毒症中线粒体功能障碍和mtDNA释放的病理生理机制以及当前的研究现状，以便为脓毒症诱导的ALI的评估、治疗和预防提供方向。
