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中华卫生应急电子杂志 ›› 2022, Vol. 08 ›› Issue (04) : 235 -236. doi: 10.3877/cma.j.issn.2095-9133.2022.04.009

综述

TLR4炎症通路在脓毒症心肌损伤中的调控作用
迪丽热巴·吐尔逊1, 丁琼莉1, 于湘友1,()   
  1. 1. 830054 新疆乌鲁木齐,新疆医科大学第一附属医院重症医学科
  • 收稿日期:2022-06-10 出版日期:2022-08-18
  • 通信作者: 于湘友
  • 基金资助:
    国家自然科学基金(82160360)

Regulation of TLR4 inflammatory pathway in sepsis-induced myocardial injury

Tuerxun Dilireba·1, Qiongli Ding1, Xiangyou Yu1()   

  • Received:2022-06-10 Published:2022-08-18
  • Corresponding author: Xiangyou Yu
引用本文:

迪丽热巴·吐尔逊, 丁琼莉, 于湘友. TLR4炎症通路在脓毒症心肌损伤中的调控作用[J]. 中华卫生应急电子杂志, 2022, 08(04): 235-236.

Tuerxun Dilireba·, Qiongli Ding, Xiangyou Yu. Regulation of TLR4 inflammatory pathway in sepsis-induced myocardial injury[J]. Chinese Journal of Hygiene Rescue(Electronic Edition), 2022, 08(04): 235-236.

Toll样受体(toll-like receptors,TLRs)是人体获得性免疫系统中具有识别作用的一类跨膜受体,能够识别并结合多种病原体相关分子模式(pathogen-associated molecular pattern,PAMP)[1],其引起的细胞内信号转导途径导致核转录因子κB(nuclear factor-κB,NF-κB)通路的激活,引起先天性免疫反应和炎症介质表达[2]。TLR家族中的Toll样受体4(toll-like receptors 4,TLR4)是脂多糖(lipopolysaccharide,LPS)的主要受体蛋白,可使其水平上调,进而激活TLR4下游的髓样分化蛋白88(myeloid differentiation factor88,MyD88)途径,两者通过同源结构域相互作用,引起信号级联最终导致核因子NF-kB通路活化,诱导产生TNF-α、IL-1β、IL-6以及趋化型细胞因子,从而介导炎症反应的发生[3,4]。脓毒症心肌病(septic cardiomyopathy,SCM)是严重脓毒症常见的重要并发症之一,可使脓毒症患者病死率增加20%~50%[5]。在分子机制的研究中,TLR4/MyD88/NF-κB炎症信号通路在脓毒症心肌炎性损伤中发挥着至关重要的作用。因此,笔者对TLR4炎症通路在脓毒症心肌病中的调控作用进行综述。

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