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Sepsis-induced myocardial dysfunction: the role of mitochondrial dysfunction
Inflammation Research ( IF 6.7 ) Pub Date : 2021-03-08 , DOI: 10.1007/s00011-021-01447-0
Hang Yang 1 , Zhaocai Zhang 2
Affiliation  

Introduction

Sepsis-induced myocardial dysfunction (SIMD) is a condition manifested by an intrinsic myocardial systolic and diastolic dysfunction during sepsis, which is associated with worse clinical outcomes and a higher mortality.

Materials and methods

Several pathophysiological mechanisms including mitochondrial dysfunction, abnormal body immune reaction, metabolic reprogramming, excessive production of reactive oxygen species (ROS), and disorder of calcium regulation have been involved in SIMD. Mitophagy has potential role in protecting myocardial cells in sepsis, especially in survivors.

Conclusion

In the current review, we focus on the role of mitochondrial dysfunction and other mitochondria-related mechanisms including immunologic imbalance, energetic reprogramming, mitophagy, and pyroptosis in the mechanisms of SIMD.



中文翻译:

脓毒症引起的心肌功能障碍:线粒体功能障碍的作用

介绍

脓毒症诱导的心肌功能障碍 (SIMD) 是一种在脓毒症期间表现为内在心肌收缩和舒张功能障碍的病症,这与更差的临床结果和更高的死亡率有关。

材料和方法

SIMD 涉及多种病理生理机制,包括线粒体功能障碍、身体免疫反应异常、代谢重编程、活性氧 (ROS) 过度产生和钙调节紊乱。Mitophagy 在保护败血症心肌细胞方面具有潜在作用,尤其是在幸存者中。

结论

在当前的综述中,我们关注线粒体功能障碍和其他线粒体相关机制,包括免疫失衡、能量重编程、线粒体自噬和细胞焦亡在 SIMD 机制中的作用。

更新日期:2021-03-08
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