Department of Gastrointestinal Surgery II, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, P.R. China.
Mol Med Rep. 2022 Apr;25(4). doi: 10.3892/mmr.2022.12663. Epub 2022 Mar 2.
Mitochondria are key organelles of cellular energy metabolism; both mitochondrial function and metabolism determine the physiological function of cells and serve an essential role in immune responses. Key damage‑associated molecular patterns (DAMPs), such as mitochondrial DNA and N‑formyl peptides, released following severe trauma‑induced mitochondrial damage may affect the respiratory chain, enhance oxidative stress and activate systemic inflammatory responses via a variety of inflammation‑associated signaling pathways. Severe trauma can lead to sepsis, multiple organ dysfunction syndrome and death. The present review aimed to summarize the pathophysiological mechanisms underlying the effects of human mitochondrial injury‑released DAMPs on triggering systemic inflammatory responses and to determine their potential future clinical applications in preventing and treating sepsis.
线粒体是细胞能量代谢的关键细胞器；线粒体的功能和代谢决定了细胞的生理功能，在免疫反应中起着至关重要的作用。严重创伤诱导的线粒体损伤后释放的主要损伤相关分子模式（DAMPs），如线粒体 DNA 和 N-甲酰肽，可能通过多种炎症相关信号通路影响呼吸链、增强氧化应激并激活全身炎症反应。严重创伤可导致脓毒症、多器官功能障碍综合征和死亡。本综述旨在总结人线粒体损伤释放 DAMPs 触发全身炎症反应的病理生理机制，并确定其在预防和治疗脓毒症方面的潜在临床应用。
