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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。

相似文献

[1]
RNA m6A methylation regulators in sepsis.

Mol Cell Biochem. 2024-9

[2]
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[3]
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[4]
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[5]
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[6]
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[7]
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[8]
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[9]
Fusaric acid decreases p53 expression by altering promoter methylation and m6A RNA methylation in human hepatocellular carcinoma (HepG2) cells.

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[10]
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引用本文的文献

[1]
METTL14 Hinders DCM Progression via Mediating the m6A Methylation of NRG4 in HG-Induced H9C2 Cells.

Mol Biotechnol. 2025-9-2

[2]
m6A modification of non‑coding RNA: Mechanisms, functions and potential values in human diseases (Review).

Int J Mol Med. 2025-10

[3]
RNA Modification in Metabolism.

MedComm (2020). 2025-3-10

[4]
m6A RNA methylation: a pivotal regulator of tumor immunity and a promising target for cancer immunotherapy.

J Transl Med. 2025-2-28

[5]
Exploring m6A modifications in gastric cancer: from molecular mechanisms to clinical applications.

Eur J Med Res. 2025-2-12

[6]
Dexmedetomidine plays a protective role in sepsis-associated myocardial injury by repressing PRMT5-mediated ferroptosis.

Toxicol Res (Camb). 2025-2-2

[7]
Triple‑negative breast cancer cell‑derived piR‑31115 promotes the proliferation and migration of endothelial cells via METTL3‑mediated m6A modification of YAP1.

Oncol Rep. 2025-3

[8]
Identification of lethality-related m7G methylation modification patterns and the regulatory features of immune microenvironment in sepsis.

Heliyon. 2024-12-4

[9]
METTL3 accelerates staphylococcal protein A (SpA)-induced osteomyelitis progression by regulating m6A methylation-modified miR-320a.

J Orthop Surg Res. 2024-11-6

[10]
ALKBH5 Stabilized N-Methyladenosine-Modified LOC4191 to Suppress -Induced Apoptosis.

Cells. 2023-11-10

本文引用的文献

[1]
METTL3-mediated m6A mRNA methylation regulates neutrophil activation through targeting TLR4 signaling.

Cell Rep. 2023-3-28

[2]
SILENCING M 6 A READER YTHDC1 REDUCES INFLAMMATORY RESPONSE IN SEPSIS-INDUCED CARDIOMYOPATHY BY INHIBITING SERPINA3N EXPRESSION.

Shock. 2023-5-1

[3]
N-methyladenosine of Spi2a attenuates inflammation and sepsis-associated myocardial dysfunction in mice.

Nat Commun. 2023-3-2

[4]
Ythdf2 promotes pulmonary hypertension by suppressing Hmox1-dependent anti-inflammatory and antioxidant function in alveolar macrophages.

Redox Biol. 2023-5

[5]
N6-methyladenosine writer METTL3 accelerates the sepsis-induced myocardial injury by regulating m6A-dependent ferroptosis.

Apoptosis. 2023-4

[6]
Emodin accelerates diabetic wound healing by promoting anti-inflammatory macrophage polarization.

Eur J Pharmacol. 2022-12-5

[7]
The RNA mA writer WTAP in diseases: structure, roles, and mechanisms.

Cell Death Dis. 2022-10-7

[8]
Role of WTAP in Cancer: From Mechanisms to the Therapeutic Potential.

Biomolecules. 2022-9-2

[9]
N-methyladenosine (mA) methyltransferase METTL3 regulates sepsis-induced myocardial injury through IGF2BP1/HDAC4 dependent manner.

Cell Death Discov. 2022-7-15

[10]
mA demethylase ALKBH5 is required for antibacterial innate defense by intrinsic motivation of neutrophil migration.

Signal Transduct Target Ther. 2022-6-29

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