Jin Shanzi, Wang Sheng
Department of Critical Care Medicine, Tenth People's Hospital of Tongji University, Shanghai 200072, China. Corresponding author: Wang Sheng, Email:
Zhonghua Wei Zhong Bing Ji Jiu Yi Xue. 2016 Aug;28(8):747-51. doi: 10.3760/cma.j.issn.2095-4352.2016.08.018.
Sepsis is defined as life-threatening organ dysfunction caused by a dys-regulated host response to infection and septic myocardial depression (SMD) is a common complication. Pathogenesis of SMD is complicated and there is lack of specific treatment. Mitochondrial damage is an important pathological basis of SMD, and mitochondrial permeability transition pore (MPTP) plays an important role in maintaining the normal structure and function of the mitochondria. The change of MPTP during sepsis is summarized in this review so as to reveal the significant mechanism of MPTP in the occurrence of SMD.
脓毒症被定义为由宿主对感染的失调反应引起的危及生命的器官功能障碍，而脓毒症性心肌抑制（SMD）是一种常见并发症。SMD的发病机制复杂，且缺乏特异性治疗方法。线粒体损伤是SMD的重要病理基础，线粒体通透性转换孔（MPTP）在维持线粒体的正常结构和功能中起重要作用。本文综述了脓毒症期间MPTP的变化，以揭示MPTP在SMD发生中的重要机制。
