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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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[1]
m6A RNA modification pathway: orchestrating fibrotic mechanisms across multiple organs.

Brief Funct Genomics. 2025-1-15

[2]
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Exp Neurol. 2021-11

[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]
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[10]
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[1]
Photosensitive and dual-targeted chromium nanoparticle delivering small interfering RNA YTHDF1 for molecular-targeted immunotherapy in liver cancer.

J Nanobiotechnology. 2024-6-19

[2]
ALKBH5-mediated m6A modification of IL-11 drives macrophage-to-myofibroblast transition and pathological cardiac fibrosis in mice.

Nat Commun. 2024-3-5

[3]
Targeting the mA RNA methyltransferase METTL3 attenuates the development of kidney fibrosis.

Exp Mol Med. 2024-2

[4]
YTHDC1 delays cellular senescence and pulmonary fibrosis by activating ATR in an m6A-independent manner.

EMBO J. 2024-1

[5]
TNC Accelerates Hypoxia-Induced Cardiac Injury in a METTL3-Dependent Manner.

Genes (Basel). 2023-2-26

[6]
METTL3-mediated m6A modification of HMGA2 mRNA promotes subretinal fibrosis and epithelial-mesenchymal transition.

J Mol Cell Biol. 2023-8-3

[7]
N-methyladenosine mediates Nrf2 protein expression involved in PM2.5-induced pulmonary fibrosis.

Ecotoxicol Environ Saf. 2023-4-1

[8]
Inhibition of ALKBH5 attenuates I/R-induced renal injury in male mice by promoting Ccl28 m6A modification and increasing Treg recruitment.

Nat Commun. 2023-3-1

[9]
DNA 5mC and RNA mA modification successively facilitates the initiation and perpetuation stages of HSC activation in liver fibrosis progression.

Cell Death Differ. 2023-5

[10]
mA methylation-induced NR1D1 ablation disrupts the HSC circadian clock and promotes hepatic fibrosis.

Pharmacol Res. 2023-3

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