线粒体是心肌能量代谢的主要场所也是脓毒症心肌损伤(sepsis-induced myocardial injury,SIMI)的关键参与者。本文主要从线粒体功能异常和结构异常两个方面综述了参与SIMI的线粒体损伤机制,包括氧化应激、钙离子超载、线粒体通透性转换孔的过度激活、线粒体动力学变化以及线粒体自噬等。此外,文章还探讨了对抗线粒体损伤的研究进展,旨在为SIMI的治疗提供新的思路。
Mitochondria are the main sites of myocardial energy metabolism and key players in sepsis-induced myocardial injury. This article primarily reviews the mechanisms of mitochondrial damage involved in SIMI from two aspects: mitochondrial dysfunc-tion and structural disorder. It includes oxidative stress, Ca2+ overload, overactivation of mitochondrial permeability transition pores, changes in mitochondrial dynamics, mitophagy. Additionally, the article discusses the research progress in combating mitochondrial damage, hoping to provide new ideas for the treatment of SIMI.
Cited