TFEB与线粒体稳态在脓毒症并发症中的调控机制  

Regulation of TFEB and mitochondrial homeostasis during sepsis complications

作　　者：李钰 赵倩倩 梁胜贤 钟理[1,2] 郭蕊 LI Yu;ZHAO QianQian;LIANG ShengXian;ZHONG Li;GUO Rui(Stem Cell and Biomedical Research Laboratory,School of Life Sciences,Hebei University,Baoding 071002,China;Institute of Life Science and Green Development,Hebei University,Baoding 071002,China)

机构地区：[1]河北大学生命科学学院干细胞与生物医学研究实验室,保定071002 [2]河北大学生命科学与绿色发展研究院,保定071002

出　　处：《中国科学：生命科学》2021年第9期1208-1217,共10页Scientia Sinica(Vitae)

基　　金：国家自然科学基金(批准号:31900534);河北省自然科学基金(批准号:C2019201349);河北省百人计划资助项目(批准号:E2019050010);河北大学高层次人才培养计划专项(批准号:801260201282)资助。

摘　　要：脓毒症是由宿主感染引起的炎症反应综合征,伴随着多器官功能障碍,对心血管系统的影响尤为显著.脓毒症患者心肌功能障碍包括炎症、线粒体功能紊乱、氧化应激、低代谢等.线粒体稳态是维持机体健康的重要基础,线粒体功能障碍会引发心肌炎症甚至心力衰竭.转录因子EB(transcription factor EB,TFEB)是调控自噬和溶酶体生物发生的关键转录因子,在线粒体自噬和线粒体生物发生,以及心血管的稳态调控中发挥至关重要的作用.本文总结了近年来脓毒症中TFEB与线粒体调控和功能的研究进展,并讨论了TFEB在细胞内稳态和脓毒症并发症中的潜在作用.Sepsis is an inflammatory response syndrome caused by host infection.It is accompanied by multiple organ dysfunction,which has a significant impact on the cardiovascular system.Myocardial dysfunction in patients with sepsis includes inflammation,mitochondrial disorder,oxidative stress,and low metabolism.Mitochondrial dysfunction can cause myocardial inflammation and even heart failure.Transcription factor EB(TFEB),a transcription factor that regulates autophagy and lysosomal biogenesis,acts as an important regulator for maintaining cardiovascular homeostasis.It plays an essential role in the regulation of mitochondrial biogenesis and mitophagy to maintain cellular homeostasis.In this article,we summarize the recent research progress made in understanding TFEB and its role in regulating mitochondrial function in sepsis.We also discuss the potential role of TFEB in cellular homeostasis during septic complications.

关 键 词：TFEB 线粒体 自噬 心血管损伤 脓毒症 炎症 

分 类 号：R459.7[医药卫生—急诊医学]