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脓毒症中的 RNA m6A 甲基化调节因子。

RNA m6A methylation regulators in sepsis.

机构信息

School of Chinese Medicine, Shandong University of Traditional Chinese Medicine, Jinan, People's Republic of China.

Department of Obstetrics and Gynecology, Shandong Provincial Third Hospital, Jinan, 250031, People's Republic of China.

出版信息

Mol Cell Biochem. 2024 Sep;479(9):2165-2180. doi: 10.1007/s11010-023-04841-w. Epub 2023 Sep 2.

DOI:10.1007/s11010-023-04841-w
PMID:37659034
Abstract

N6-methyladenosine (m6A) modification is a class of epitope modifications that has received significant attention in recent years, particularly in relation to its role in various diseases, including sepsis. Epigenetic research has increasingly focused on m6A modifications, which is influenced by the dynamic regulation of three protein types: ‟Writers" (such as METTL3/METTL14/WTAP)-responsible for m6A modification; ‟Erasers" (FTO and ALKBH5)-involved in m6A de-modification; and ‟Readers" (YTHDC1/2, YTHDF1/2/3)-responsible for m6A recognition. Sepsis, a severe and fatal infectious disease, has garnered attention regarding the crucial effect of m6A modifications on its development. In this review, we attempted to summarize the recent studies on the involvement of m6A and its regulators in sepsis, as well as the significance of m6A modifications and their regulators in the development of novel drugs and clinical treatment. The potential value of m6A modifications and modulators in the diagnosis, treatment, and prognosis of sepsis has also been discussed.

摘要

N6-甲基腺苷(m6A)修饰是一类被广泛关注的表位修饰,其在各种疾病中的作用,特别是在败血症中的作用,受到了广泛关注。表观遗传学研究越来越关注 m6A 修饰,其受到三种蛋白质类型的动态调控:“writers”(如 METTL3/METTL14/WTAP)——负责 m6A 修饰;“erasers”(FTO 和 ALKBH5)——参与 m6A 去修饰;“readers”(YTHDC1/2、YTHDF1/2/3)——负责 m6A 识别。败血症是一种严重且致命的传染病,其发展过程中 m6A 修饰的关键作用受到了关注。在这篇综述中,我们试图总结 m6A 及其调控因子在败血症中的作用的最新研究,以及 m6A 修饰及其调控因子在新型药物开发和临床治疗中的意义。还讨论了 m6A 修饰和调节剂在败血症的诊断、治疗和预后中的潜在价值。

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METTL3-mediated m6A mRNA methylation regulates neutrophil activation through targeting TLR4 signaling.METTL3介导的m6A mRNA甲基化通过靶向TLR4信号传导调节中性粒细胞活化。
Cell Rep. 2023 Mar 28;42(3):112259. doi: 10.1016/j.celrep.2023.112259. Epub 2023 Mar 14.
2
SILENCING M 6 A READER YTHDC1 REDUCES INFLAMMATORY RESPONSE IN SEPSIS-INDUCED CARDIOMYOPATHY BY INHIBITING SERPINA3N EXPRESSION.沉默 M6A 读码子 YTHDC1 通过抑制 SERPA3N 表达减少脓毒症诱导性心肌病中的炎症反应。
Shock. 2023 May 1;59(5):791-802. doi: 10.1097/SHK.0000000000002106. Epub 2023 Mar 7.
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N-methyladenosine of Spi2a attenuates inflammation and sepsis-associated myocardial dysfunction in mice.
MedComm (2020). 2025 Mar 10;6(3):e70135. doi: 10.1002/mco2.70135. eCollection 2025 Mar.
4
m6A RNA methylation: a pivotal regulator of tumor immunity and a promising target for cancer immunotherapy.m6A RNA甲基化:肿瘤免疫的关键调节因子及癌症免疫治疗的潜在靶点
J Transl Med. 2025 Feb 28;23(1):245. doi: 10.1186/s12967-025-06221-y.
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Exploring m6A modifications in gastric cancer: from molecular mechanisms to clinical applications.探索胃癌中的m6A修饰:从分子机制到临床应用
Eur J Med Res. 2025 Feb 12;30(1):98. doi: 10.1186/s40001-025-02353-5.
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