Zhan Biao, Shen Jie
Center of Emergency and Critical Medicine, Jinshan Hospital of Fudan University, Shanghai 201508, P.R. China.
Research Center for Chemical Injury, Emergency and Critical Medicine of Fudan University, Shanghai 201508, P.R. China.
Exp Ther Med. 2022 Jun 1;24(1):479. doi: 10.3892/etm.2022.11406. eCollection 2022 Jul.
Acute lung injury (ALI) and its more serious form [acute respiratory distress syndrome (ARDS)] are devastating diseases that lead to high morbidity and mortality rates in patients in intensive care units. ALI is caused by numerous direct or indirect factors, including trauma and sepsis. However, the underlying mechanism associated with the pathophysiological process of ALI has yet to be fully elucidated. As our understanding of mitochondrial biology continuously progresses, mitochondria have been largely considered as biosynthetic, bioenergetic and signaling organelles that have a critical role in the processes of cellular development, proliferation and death, and novel insights into how mitochondrial dysfunction affects the pathogenesis of different diseases have been garnered. According to current research models, functional characteristics of mitochondria are recognized to affect the function of cells and organs in ALI. The aim of the present review is therefore to discuss mitochondria and their role in ALI, and to consider how they may serve as potential therapeutic targets for this disease.
急性肺损伤（ALI）及其更严重的形式[急性呼吸窘迫综合征（ARDS）]是极具破坏性的疾病，会导致重症监护病房患者的高发病率和死亡率。ALI由多种直接或间接因素引起，包括创伤和脓毒症。然而，与ALI病理生理过程相关的潜在机制尚未完全阐明。随着我们对线粒体生物学的理解不断深入，线粒体在很大程度上已被视为在细胞发育、增殖和死亡过程中起关键作用的生物合成、生物能量和信号细胞器，并且已获得了关于线粒体功能障碍如何影响不同疾病发病机制的新见解。根据当前的研究模型，线粒体的功能特性被认为会影响ALI中细胞和器官的功能。因此，本综述的目的是讨论线粒体及其在ALI中的作用，并考虑它们如何可能成为该疾病的潜在治疗靶点。
