Abstract

肝衰竭是临床上常见的终末期肝病症候群,其特征是肝细胞大量坏死导致肝功能迅速衰竭,目前认为其核心机制是过度炎症和免疫反应等。内源性脂质介质参与了多种炎症过程的调节,包括启动、维持和消退,其中类二十烷酸和促分解脂质介质及其复杂的代谢途径和传导信号在这些过程的调节中起关键作用。本文综述了内源性脂质介质在肝衰竭炎症及免疫功能障碍病理生理机制中的关键作用,以及通过脂质免疫途径在肝衰竭中的潜在意义和治疗的新机会,以期为肝衰竭的临床诊疗提供新思路。

Alternate abstract:

Liver failure is a common end-stage liver disease syndrome in clinical practice characterized by massive necrosis of hepatocytes leading to rapid liver failure, and it is currently believed that excessive inflammation and immune response are the core mechanisms of this disease. Endogenous lipid mediators are involved in the regulation of a variety of inflammatory processes, including initiation, maintenance, and regression, and eicosanoids and pro-decomposition lipid mediators, as well as their complex metabolic pathways and transduction signals, play a key role in the regulation of these processes. This article reviews the key role of endogenous lipid mediators in the pathophysiological mechanism of inflammation and immune dysfunction in liver failure and the potential significance and new therapeutic opportunities of lipid immune pathway in liver failure, in order to provide new ideas for the clinical diagnosis and treatment of liver failure.

Details

Title
内源性脂质介质在肝衰竭中的应用及潜在价值
Author
颜耿杰; 林镛; 苏会吉; 陈含笑; 班少群; 韦艾凌; 毛德文; 龙富立  VIAFID ORCID Logo 
Pages
211-217
Section
Review
Publication year
2023
Publication date
2023
Publisher
Journal of Clinical Hepatology
ISSN
10015256
e-ISSN
20973497
Source type
Scholarly Journal
Language of publication
Chinese
ProQuest document ID
3239118069
Copyright
© 2023. This work is published under https://creativecommons.org/licenses/by-nc-nd/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.