m6A modification in non-coding RNAs: Mechanisms and potential therapeutic implications in fibrosis - 20/09/24
Abstract |
N6-methyladenosine (m 6 A) 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. m 6 A catalyzes messenger RNA(mRNA) as well as regulatory non-coding RNAs (ncRNAs), such as microRNAs, long non-coding RNAs, and circular RNAs. This modification modulates ncRNA fate and cell functions in various bioprocesses, including ncRNA splicing, maturity, export, and stability. Key m 6 A regulators, including writers, erasers, and readers, have been reported to modify the ncRNAs involved in fibrogenesis. NcRNAs affect fibrosis progression by targeting m 6 A regulators. The interactions between m 6 A and ncRNAs can influence multiple cellular life activities. In this review, we discuss the impact of the interaction between m 6 A modifications and ncRNAs on the pathological mechanisms of fibrosis, revealing the possibility of these interactions as diagnostic markers and therapeutic targets in fibrosis.
Le texte complet de cet article est disponible en PDF.Graphical Abstract |
Highlights |
• | Fibrosis development includes inflammation and abnormal cell transformation. |
• | m 6 A methylation is reversible and consists of writers, erasers, and readers. |
• | m 6 A modification regulates non-coding RNAs through maturity, splicing, and stability. |
• | Non-coding RNAs modulate m 6 A regulators to regulate m 6 A modification process. |
• | The interactions between m 6 A modifications and non-coding RNAs in fibrosis. |
Keywords : M 6 A RNA methylation , Noncoding RNAs, Fibrosis
Plan
Vol 179
Article 117331- octobre 2024 Retour au numéroBienvenue sur EM-consulte, la référence des professionnels de santé.
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