Department of Gastroenterology, West China Hospital, Sichuan University, No. 37, Guo Xue Xiang, Wu Hou District, Chengdu, 610041, China.
Department of Critical Care Medicine, Second Affiliated Hospital, School of Medicine, Zhejiang University, Jiefang Road No. 88, Hangzhou, 310000, Zhejiang province, China.
Inflamm Res. 2021 Apr;70(4):379-387. doi: 10.1007/s00011-021-01447-0. Epub 2021 Mar 8.
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.
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.
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.
脓毒症引起的心肌功能障碍（SIMD）是一种在脓毒症期间表现出固有心肌收缩和舒张功能障碍的病症，与更差的临床结局和更高的死亡率相关。
几种病理生理机制，包括线粒体功能障碍、异常的全身免疫反应、代谢重编程、活性氧（ROS）的过度产生以及钙调节紊乱，都与 SIMD 有关。自噬在脓毒症中心肌细胞的保护中具有潜在作用，特别是在幸存者中。
在本综述中，我们重点关注线粒体功能障碍以及其他与线粒体相关的机制，包括免疫失衡、能量重编程、自噬和细胞焦亡在 SIMD 机制中的作用。
