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m6A RNA修饰途径:协调多个器官的纤维化机制

m6A RNA modification pathway: orchestrating fibrotic mechanisms across multiple organs.

作者信息

Huang Xiangfei, Yu Zilu, Tian Juan, Chen Tao, Wei Aiping, Mei Chao, Chen Shibiao, Li Yong

机构信息

Department of Anesthesiology, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, 17 Yongwaizheng Street, Donghu District, Nanchang 330006, China.

Queen Mary School, Medical College, Nanchang University, 1299 Xuefu Road, Honggutan District, Nanchang 330031, China.

出版信息

Brief Funct Genomics. 2025 Jan 15;24. doi: 10.1093/bfgp/elae051.

DOI:10.1093/bfgp/elae051
PMID:39756462
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11735750/
Abstract

Organ fibrosis, a common consequence of chronic tissue injury, presents a significant health challenge. Recent research has revealed the regulatory role of N6-methyladenosine (m6A) RNA modification in fibrosis of various organs, including the lung, liver, kidney, and heart. In this comprehensive review, we summarize the latest findings on the mechanisms and functions of m6A modification in organ fibrosis. By highlighting the potential of m6A modification as a therapeutic target, our goal is to encourage further research in this emerging field and support advancements in the clinical treatment of organ fibrosis.

摘要

器官纤维化是慢性组织损伤的常见后果,对健康构成重大挑战。最近的研究揭示了N6-甲基腺苷(m6A)RNA修饰在包括肺、肝、肾和心脏在内的各种器官纤维化中的调节作用。在这篇综述中,我们总结了m6A修饰在器官纤维化中的机制和功能的最新发现。通过强调m6A修饰作为治疗靶点的潜力,我们的目标是鼓励在这个新兴领域进行进一步研究,并支持器官纤维化临床治疗的进展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0441/11735750/74f15a6a2d08/elae051f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0441/11735750/b6754349d20d/elae051f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0441/11735750/74f15a6a2d08/elae051f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0441/11735750/b6754349d20d/elae051f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0441/11735750/74f15a6a2d08/elae051f2.jpg

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J Nanobiotechnology. 2024 Jun 19;22(1):348. doi: 10.1186/s12951-024-02612-3.
2
ALKBH5-mediated m6A modification of IL-11 drives macrophage-to-myofibroblast transition and pathological cardiac fibrosis in mice.ALKBH5 介导的 IL-11 的 m6A 修饰驱动小鼠巨噬细胞向肌成纤维细胞转化和病理性心脏纤维化。
Nat Commun. 2024 Mar 5;15(1):1995. doi: 10.1038/s41467-024-46357-x.
3
Targeting the mA RNA methyltransferase METTL3 attenuates the development of kidney fibrosis.
靶向 mA RNA 甲基转移酶 METTL3 可减轻肾脏纤维化的发展。
Exp Mol Med. 2024 Feb;56(2):355-369. doi: 10.1038/s12276-024-01159-5. Epub 2024 Feb 1.
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YTHDC1 delays cellular senescence and pulmonary fibrosis by activating ATR in an m6A-independent manner.YTHDC1 通过非依赖于 m6A 的方式激活 ATR 来延缓细胞衰老和肺纤维化。
EMBO J. 2024 Jan;43(1):61-86. doi: 10.1038/s44318-023-00003-2. Epub 2023 Dec 15.
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TNC Accelerates Hypoxia-Induced Cardiac Injury in a METTL3-Dependent Manner.TNC 以 METTL3 依赖的方式加速低氧诱导的心脏损伤。
Genes (Basel). 2023 Feb 26;14(3):591. doi: 10.3390/genes14030591.
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METTL3-mediated m6A modification of HMGA2 mRNA promotes subretinal fibrosis and epithelial-mesenchymal transition.METTL3 介导的 HMGA2 mRNA m6A 修饰促进视网膜下纤维化和上皮-间充质转化。
J Mol Cell Biol. 2023 Aug 3;15(3). doi: 10.1093/jmcb/mjad005.
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Ecotoxicol Environ Saf. 2023 Apr 1;254:114755. doi: 10.1016/j.ecoenv.2023.114755. Epub 2023 Mar 12.
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Pharmacol Res. 2023 Mar;189:106704. doi: 10.1016/j.phrs.2023.106704. Epub 2023 Feb 20.