m6A modification in non-coding RNAs: Mechanisms and potential therapeutic implications in fibrosis

被引:1
|
作者
Zhou, Yutong [1 ]
Jian, Ni [1 ]
Jiang, Canhua [2 ]
Wang, Jie [1 ]
机构
[1] Cent South Univ, Xiangya Sch Med, Dept Immunol, Changsha 410078, Peoples R China
[2] Cent South Univ, Xiangya Hosp, Dept Oral & Maxillofacial Surg, Changsha 410078, Peoples R China
基金
中国国家自然科学基金;
关键词
M 6 A RNA methylation; Noncoding RNAs; Fibrosis; MESSENGER-RNA; NUCLEAR-RNA; PULMONARY-FIBROSIS; CARDIAC FIBROSIS; RENAL FIBROSIS; CIRCULAR RNAS; TRANSLATION; DIFFERENTIATION; DECAY; BETA;
D O I
10.1016/j.biopha.2024.117331
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
N6-methyladenosine (m6A) is one of the most prevalent and reversible forms of RNA methylation, with increasing evidence indicating its critical role in numerous physiological and pathological processes. m6A catalyzes messenger RNA(mRNA) as well as regulatory non-coding RNAs (ncRNAs), such as microRNAs, long noncoding RNAs, and circular RNAs. This modification modulates ncRNA fate and cell functions in various bioprocesses, including ncRNA splicing, maturity, export, and stability. Key m6A regulators, including writers, erasers, and readers, have been reported to modify the ncRNAs involved in fibrogenesis. NcRNAs affect fibrosis progression by targeting m6A regulators. The interactions between m6A and ncRNAs can influence multiple cellular life activities. In this review, we discuss the impact of the interaction between m6A modifications and ncRNAs on the pathological mechanisms of fibrosis, revealing the possibility of these interactions as diagnostic markers and therapeutic targets in fibrosis.
引用
收藏
页数:11
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