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m6A修饰:一种通过巨噬细胞极化调节动脉粥样硬化的新机制。

m6A modification: a novel mechanism that regulates atherosclerosis via macrophage polarization.

作者信息

Li Xiaying, Zhang Hengkai, Zhou Yan, Zhang Lei, Huang Ye

机构信息

Graduate School, Beijing University of Chinese Medicine, Beijing, China.

Emergency Department, Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing, China.

出版信息

Front Immunol. 2025 Jun 16;16:1607932. doi: 10.3389/fimmu.2025.1607932. eCollection 2025.

DOI:10.3389/fimmu.2025.1607932
PMID:40589753
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12206623/
Abstract

Atherosclerosis is a chronic vascular inflammatory disease in which macrophages play a pivotal role in modulating its pathology. In response to the intraplaque microenvironment, both pro-inflammatory M1 and anti-inflammatory M2 phenotypes of macrophages have the polarization capability, each influencing the inflammatory state through the secretion of distinct cytokines. N6-methyladenosine (m6A) modification, the most prevalent internal chemical modification of RNA, significantly impacts various biological processes, including RNA transcription and protein expression. m6A modification acts as a critical determinant in macrophage polarization, with its molecular mechanisms intricately linked to the progression of atherosclerosis. This review aims to elucidate how different macrophage polarization phenotypes influence the progression of atherosclerosis while also exploring the significance of m6A modifications in this pathological context, thereby providing a theoretical foundation for identifying novel diagnostic and therapeutic targets for atherosclerosis.

摘要

动脉粥样硬化是一种慢性血管炎症性疾病,其中巨噬细胞在调节其病理过程中起关键作用。响应斑块内微环境,巨噬细胞的促炎M1型和抗炎M2型均具有极化能力,每种类型通过分泌不同的细胞因子影响炎症状态。N6-甲基腺苷(m6A)修饰是RNA最普遍的内部化学修饰,显著影响包括RNA转录和蛋白质表达在内的各种生物学过程。m6A修饰是巨噬细胞极化的关键决定因素,其分子机制与动脉粥样硬化的进展密切相关。本综述旨在阐明不同的巨噬细胞极化表型如何影响动脉粥样硬化的进展,同时探讨m6A修饰在这一病理背景下的意义,从而为确定动脉粥样硬化的新型诊断和治疗靶点提供理论基础。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/10fe/12206623/0d67eed44c56/fimmu-16-1607932-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/10fe/12206623/0d67eed44c56/fimmu-16-1607932-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/10fe/12206623/0d67eed44c56/fimmu-16-1607932-g001.jpg

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本文引用的文献

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Macrophage polarization and metabolism in atherosclerosis.动脉粥样硬化中的巨噬细胞极化和代谢。
Cell Death Dis. 2023 Oct 20;14(10):691. doi: 10.1038/s41419-023-06206-z.
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ALKBH5 inhibits TNF-α-induced apoptosis of HUVECs through Bcl-2 pathway.ALKBH5通过Bcl-2途径抑制TNF-α诱导的人脐静脉内皮细胞凋亡。
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N6-Methyladenosine Demethylase FTO (Fat Mass and Obesity-Associated Protein) as a Novel Mediator of Statin Effects in Human Endothelial Cells.
N6-甲基腺苷去甲基化酶FTO(脂肪量与肥胖相关蛋白)作为他汀类药物在人内皮细胞中作用的新型介质。
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Hemangiosarcoma cells induce M2 polarization and PD-L1 expression in macrophages.血管肉瘤细胞诱导巨噬细胞 M2 极化和 PD-L1 表达。
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ALKBH5 Regulates SPHK1-Dependent Endothelial Cell Angiogenesis Following Ischemic Stress.ALKBH5在缺血应激后调节鞘氨醇激酶1依赖的内皮细胞血管生成。
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MA methylation-mediated elevation of SM22α inhibits the proliferation and migration of vascular smooth muscle cells and ameliorates intimal hyperplasia in type 2 diabetes mellitus.MA甲基化介导的SM22α升高抑制血管平滑肌细胞的增殖和迁移,并改善2型糖尿病的内膜增生。
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m6A Modification: A Double-Edged Sword in Tumor Development.m6A修饰:肿瘤发展中的双刃剑
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9
The mA methyltransferase METTL3 modifies PGC-1α mRNA promoting mitochondrial dysfunction and oxLDL-induced inflammation in monocytes.m6A 甲基转移酶 METTL3 修饰 PGC-1α mRNA,促进单核细胞中线粒体功能障碍和 oxLDL 诱导的炎症。
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The mA methyltransferase METTL3 promotes hypoxic pulmonary arterial hypertension.m A 甲基转移酶 METTL3 促进低氧性肺动脉高血压。
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