TREM-1 在体外和体内脓毒性心肌脓毒症和脓毒性心肌病中的作用。

IF 4.5 2区 生物学 Q2 CELL BIOLOGY
Yongxia Chen, Lixia Mao, Songtao Liu, Shunyi Huang, Qiuyun Lin, Man Zeng, Huiyi Huang, Xiaocong Sun, Hongpeng Chen, Jiahao Huang, Gaosheng Zhou, Liehua Deng
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引用次数: 0

摘要

化脓性心肌病(SCM)是一种涉及心肌细胞脓毒症的急性心脏功能障碍。TREM-1 是细胞膜上的一种已知受体,可增强炎症反应。我们之前的研究表明,心肌细胞中的 TREM-1 通过 SMC4/NEMO 通路参与激活 NLRP3。在此,我们旨在利用Trem-1和Nlrp3基因敲除小鼠来验证TREM-1通过NLRP3对脓毒症小鼠心脏功能的影响。结果显示,TREM-1基因敲除导致下游细胞信号(包括SMC4和NLRP3)释放减少,从而导致细胞因子释放减少,心脏功能障碍得到改善。敲除 NLRP3 还能减少心肌细胞的脓毒症,提高存活率。针对 TREM-1 激活 NLRP3 及其通路的治疗可能有助于治疗或预防系统性红斑狼疮。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

The role of TREM-1 in septic myocardial pyroptosis and septic cardiomyopathy in vitro and in vivo

The role of TREM-1 in septic myocardial pyroptosis and septic cardiomyopathy in vitro and in vivo

Septic cardiomyopathy (SCM) is an acute cardiac dysfunction involving myocardial cell pyroptosis. TREM-1 is a known receptor on cell membrane that can amplify the inflammatory response. Our previous studies have shown that TREM-1 in cardiomyocytes is involved in the activation of NLRP3 through the SMC4/NEMO pathway. Here, we aimed to use Trem-1 and Nlrp3 knockout mice to verify the effect of TREM-1 through NLRP3 on cardiac function in septic mice. The results showed that TREM-1 knockout resulted in a decrease in the release of downstream cell signals, including SMC4 and NLRP3, resulting in a decrease in cytokine release and improvement of cardiac dysfunction. Knockout of NLRP3 also reduced cardiomyocyte pyroptosis and increased survival rate. The therapeutic targeting of TREM-1 activation of NLRP3 and its pathway may contribute to the treatment or prevention of SCM.

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来源期刊
CiteScore
14.70
自引率
0.00%
发文量
256
审稿时长
1 months
期刊介绍: The Journal of Cellular Physiology publishes reports of high biological significance in areas of eukaryotic cell biology and physiology, focusing on those articles that adopt a molecular mechanistic approach to investigate cell structure and function. There is appreciation for the application of cellular, biochemical, molecular and in vivo genetic approaches, as well as the power of genomics, proteomics, bioinformatics and systems biology. In particular, the Journal encourages submission of high-interest papers investigating the genetic and epigenetic regulation of proliferation and phenotype as well as cell fate and lineage commitment by growth factors, cytokines and their cognate receptors and signal transduction pathways that influence the expression, integration and activities of these physiological mediators. Similarly, the Journal encourages submission of manuscripts exploring the regulation of growth and differentiation by cell adhesion molecules in addition to the interplay between these processes and those induced by growth factors and cytokines. Studies on the genes and processes that regulate cell cycle progression and phase transition in eukaryotic cells, and the mechanisms that determine whether cells enter quiescence, proliferate or undergo apoptosis are also welcomed. Submission of papers that address contributions of the extracellular matrix to cellular phenotypes and physiological control as well as regulatory mechanisms governing fertilization, embryogenesis, gametogenesis, cell fate, lineage commitment, differentiation, development and dynamic parameters of cell motility are encouraged. Finally, the investigation of stem cells and changes that differentiate cancer cells from normal cells including studies on the properties and functions of oncogenes and tumor suppressor genes will remain as one of the major interests of the Journal.
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