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避免被肝脏困住:肝移植中的缺血再灌注损伤引发 S1P 介导的 NETosis。

Avoid being trapped by your liver: ischemia-reperfusion injury in liver transplant triggers S1P-mediated NETosis.

机构信息

Norton Thoracic Institute, St. Joseph's Hospital and Medical Center, Phoenix, Arizona, USA.

Department of Surgery, Washington University School of Medicine, St. Louis, Missouri, USA.

出版信息

J Clin Invest. 2023 Feb 1;133(3):e167012. doi: 10.1172/JCI167012.

Abstract

Liver transplantation can be a life-saving treatment for end-stage hepatic disease. Unfortunately, some recipients develop ischemia-reperfusion injury (IRI) that leads to poor short- and long-term outcomes. Recent work has shown neutrophils contribute to IRI by undergoing NETosis, a form of death characterized by DNA ejection resulting in inflammatory extracellular traps. In this issue of the JCI, Hirao and Kojima et al. report that sphingosine-1-phosphate (S1P) expression induced by liver transplant-mediated IRI triggers NETosis. They also provide evidence that neutrophil expression of the carcinoembryonic antigen-related cell adhesion molecule-1 (CC1) long isoform inhibited NETosis by controlling S1P receptor-mediated autophagic flux. These findings suggest stimulating regulatory mechanisms that suppress NETosis could be used to prevent IRI.

摘要

肝移植可以成为治疗终末期肝病的一种救命疗法。不幸的是,一些接受者会出现缺血再灌注损伤(IRI),导致短期和长期预后不良。最近的研究表明,中性粒细胞通过 NETosis 导致 IRI,NETosis 是一种以 DNA 排出导致炎症性细胞外陷阱为特征的死亡形式。在本期 JCI 中,Hirao 和 Kojima 等人报告称,肝移植介导的 IRI 诱导的鞘氨醇-1-磷酸(S1P)表达触发 NETosis。他们还提供了证据表明,中性粒细胞表达癌胚抗原相关细胞黏附分子-1(CC1)长型异构体通过控制 S1P 受体介导的自噬通量来抑制 NETosis。这些发现表明,刺激抑制 NETosis 的调节机制可用于预防 IRI。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4220/9888375/3526cde98db6/jci-133-167012-g102.jpg

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