Guo Xiaoyu, Hong Ting, Zhang Shen, Wei Yazhong, Jin Haizhen, Miao Qing, Wang Kai, Zhou Miao, Wang Chong, He Bin
Department of Critical Care Medicine, Shanghai Chest Hospital, Shanghai Jiao Tong University, Shanghai, China.
Central Laboratory of Shanghai Chest Hospital, Shanghai Jiao Tong University, Shanghai, China.
Front Cell Dev Biol. 2021 Sep 17;9:736603. doi: 10.3389/fcell.2021.736603. eCollection 2021.
Sepsis-induced cardiac injury () is one of the most common complications in the intensive care unit (ICU) with high morbidity and mortality. Mitochondrial dysfunction is one of the main reasons for , and Interleukin-13 (IL-13) is a master regulator of mitochondria biogenesis. The aim of the present study was to investigate the role of IL-13 in and explore the underlying mechanism. It was found that reactive oxygen species (ROS) production and apoptosis were significantly increased in lipopolysaccharide (LPS)-stimulated primary cardiomyocytes, which was accompanied with obvious mitochondria dysfunction. The results of RNA-sequencing (RNA-seq), mitochondrial membrane potential, fatty acid uptake and oxidation rate suggested that treatment with IL-13 could restore the function and morphology of mitochondria, indicating that it played an important role in protecting septic cardiomyocytes. These findings demonstrated that IL-13 alleviated sepsis-induced cardiac inflammation and apoptosis by improving mitochondrial fatty acid uptake and oxidation, suggesting that IL-13 may prove to be a potential promising target for treatment.
脓毒症诱导的心脏损伤（）是重症监护病房（ICU）中最常见的并发症之一，发病率和死亡率都很高。线粒体功能障碍是其主要原因之一，而白细胞介素-13（IL-13）是线粒体生物合成的主要调节因子。本研究的目的是探讨IL-13在其中的作用并探究其潜在机制。研究发现，脂多糖（LPS）刺激的原代心肌细胞中活性氧（ROS）生成和细胞凋亡显著增加，同时伴有明显的线粒体功能障碍。RNA测序（RNA-seq）、线粒体膜电位、脂肪酸摄取和氧化率的结果表明，IL-13处理可恢复线粒体的功能和形态，表明其在保护脓毒症心肌细胞中起重要作用。这些发现表明，IL-13通过改善线粒体脂肪酸摄取和氧化减轻了脓毒症诱导的心脏炎症和细胞凋亡，提示IL-13可能是脓毒症治疗的一个潜在的有前景的靶点。
