脓毒症心肌损伤的线粒体机制研究进展

Research advances on mitochondrial mechanism of sepsis‑induced myocardial injury

脓毒症是机体对于感染的失控反应所导致的威胁生命的器官功能障碍,心肌损伤是脓毒症常见的并发症,而线粒体作为心肌细胞能量供应的主要场所,其结构和功能障碍在其中起重要作用。文章旨在总结脓毒症时线粒体功能障碍而导致心肌损伤的相关机制:线粒体内活性氧产生和氧化应激、线粒体能量代谢障碍、线粒体动力学失衡、线粒体生物合成和自噬过程异常等,为脓毒症心肌损伤的临床治疗提供新思路。

Sepsis is a life‑threatening organ dysfunction caused by the host's unbalanced response to infection.Septic cardio‑myopathy is a common complication of sepsis.As the main organoid of energy supply for cardiomyocytes,the abnormal structure and dysfunction of mitochondria plays an important role in septic cardiomyopathy.This review aims to summarize the relevant mechanisms of mitochondrial dysfunction which causes myocardial injury in sepsis,including:reactive oxygen species produced and oxidative stress occurred in mitochondria,disorder energy metabolism of mitochondria,imbalanced mitochondrial dynamics,abnormal mitochondrial biosynthesis and autophagy process for providing new ideas to help the clinical treatment of septic myocardial injury.