Immune dysregulation and RNA N6-methyladenosine modification in sepsis.

IF 6.4 2区 生物学 Q1 CELL BIOLOGY Wiley Interdisciplinary Reviews: RNA Pub Date : 2023-05-01 DOI:10.1002/wrna.1764
Hongyan Chen, Xiaoting Zhang, Hao Su, Judeng Zeng, Hung Chan, Qing Li, Xiaodong Liu, Lin Zhang, William Ka Kei Wu, Matthew Tak Vai Chan, Huarong Chen
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引用次数: 4

Abstract

Sepsis is defined as life-threatening organ dysfunction caused by the host immune dysregulation to infection. It is a highly heterogeneous syndrome with complex pathophysiological mechanisms. The host immune response to sepsis can be divided into hyper-inflammatory and immune-suppressive phases which could exist simultaneously. In the initial stage, systemic immune response is activated after exposure to pathogens. Both innate and adaptive immune cells undergo epigenomic, transcriptomic, and functional reprogramming, resulting in systemic and persistent inflammatory responses. Following the hyper-inflammatory phase, the body is in a state of continuous immunosuppression, which is related to immune cell apoptosis, metabolic failure, and epigenetic reprogramming. Immunosuppression leads to increased susceptibility to secondary infections in patients with sepsis. RNA N6-Methyladenosine (m6A) has been recognized as an indispensable epitranscriptomic modification involved in both physiological and pathological processes. Recent studies suggest that m6A could reprogram both innate and adaptive immune cells through posttranscriptional regulation of RNA metabolism. Dysregulated m6A modifications contribute to the pathogenesis of immune-related diseases. In this review, we summarize immune cell changes and the potential role of m6A modification in sepsis. This article is categorized under: RNA in Disease and Development > RNA in Disease RNA Processing > RNA Editing and Modification.

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脓毒症的免疫失调和RNA n6 -甲基腺苷修饰。
脓毒症被定义为由宿主对感染免疫失调引起的危及生命的器官功能障碍。它是一种高度异质性的综合征,具有复杂的病理生理机制。宿主对脓毒症的免疫反应可分为高炎症期和免疫抑制期,两者可同时存在。在初始阶段,全身免疫反应在接触病原体后被激活。先天和适应性免疫细胞都经历表观基因组、转录组和功能重编程,导致系统性和持续性炎症反应。在高炎症期之后,机体处于持续的免疫抑制状态,这与免疫细胞凋亡、代谢衰竭和表观遗传重编程有关。免疫抑制导致脓毒症患者继发感染易感性增加。RNA n6 -甲基腺苷(m6A)已被认为是参与生理和病理过程中不可或缺的外转录组修饰。最近的研究表明,m6A可以通过转录后调控RNA代谢对先天免疫细胞和适应性免疫细胞进行重编程。失调的m6A修饰有助于免疫相关疾病的发病机制。在这篇综述中,我们总结免疫细胞的变化和m6A修饰在脓毒症中的潜在作用。本文分类为:RNA在疾病和发展> RNA在疾病中的RNA加工> RNA编辑和修饰。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
CiteScore
14.80
自引率
4.10%
发文量
67
审稿时长
6-12 weeks
期刊介绍: WIREs RNA aims to provide comprehensive, up-to-date, and coherent coverage of this interesting and growing field, providing a framework for both RNA experts and interdisciplinary researchers to not only gain perspective in areas of RNA biology, but to generate new insights and applications as well. Major topics to be covered are: RNA Structure and Dynamics; RNA Evolution and Genomics; RNA-Based Catalysis; RNA Interactions with Proteins and Other Molecules; Translation; RNA Processing; RNA Export/Localization; RNA Turnover and Surveillance; Regulatory RNAs/RNAi/Riboswitches; RNA in Disease and Development; and RNA Methods.
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