TLRs/NF-κB和MAPK信号通路在脓毒症心肌病的研究进展  

Progression in the study of the Toll/NF-κB and MAPK signaling pathways in sepsis cardiomyopathy

作　　者：乔楚珂 单鸿伟(审校)[2] QIAO Chuke;SHAN Hongwei

机构地区：[1]内蒙古医科大学第一临床医学院,呼和浩特010100 [2]内蒙古医科大学附属医院急诊科,呼和浩特010100

出　　处：《临床急诊杂志》2020年第7期590-594,共5页Journal of Clinical Emergency

基　　金：内蒙古医科大学“科技百万工程”项目(No:YKD2015KJBW016)。

摘　　要：脓毒症(sepsis)是指机体对各种感染反应失调引起的危及生命的器官功能障碍[1],具有发病率高、发病机制复杂、病情严重的和病死率高的特点,进一步可发展为严重脓毒症和脓毒性休克。心功能不全是严重脓毒症的一个临床特征,主要表现为心肌抑制,虽然往往是可逆的,但也是导致其高病死率的主要原因之一。Sepsis is a systemic inflammatory response syndrome caused by the interaction between the host’s immune system and invading pathogens.Severe cases can develop severe sepsis and septic shock.Sepsis cardiomyopathy is a reversible cardiac dysfunction characterized by enlarged left ventricle and decreased ejection fraction which can complete return to normal in 7-10 days.It is common in patients with severe sepsis and is the main cause of death.Although the exact mechanism by which sepsis causes cardiac dysfunction is unclear,TLRs act as immunomodulators to regulate specific signaling pathways during the immune response and play an important role in myocardial suppression caused by sepsis cardiomyopathy.Now relevant researches were reviewed.

关 键 词：脓毒症心肌病 TOLL样受体家族 核因子κB 丝裂原活化蛋白激酶 心肌抑制 

分 类 号：R542.2[医药卫生—心血管疾病]