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DOI 10.1002/smmd.20230008

Медицинская библиотека · Smart medicine · 2023

Roles of N6-methyladenosine epitranscriptome in non-alcoholic fatty liver disease and hepatocellular carcinoma.

Chen Yuyan, Zhu Zhengyi, Zhang Lu, Wang Jinglin, Ren Haozhen

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Non-alcoholic fatty liver disease (NAFLD) is a typical chronic liver disease connected to a high risk of developing hepatocellular carcinoma (HCC). The development of NAFLD and HCC has been associated with changes in epigenetics, such as histone modifications and micro RNA (miRNA)-mediated processes. Recently, in the realm of epitranscriptomics, RNA alterations have become important regulators. N6-methyladenosine (m6A) is the most common and crucial alteration for controlling mRNA stability, splicing, and translation. It is particularly important for controlling liver disease progression and hepatic function. This review aims to conclude recent research on the functions of m6A epitranscriptome in the molecular mechanisms behind NAFLD and HCC development, with special attention to the effects of m6A alteration on how HCC develops and its possible roles in the progression of NAFLD to HCC. Additionally, the review discusses the possible effects of m6A alteration on the treatment and diagnostic of NAFLD and HCC. It is crucial to remember that m6A modification is a reversible action controlled via the coordinated functions of the proteins that write and delete, enabling quick adaptability to environmental changes. The review also discusses m6A-binding proteins' function in mRNA alternative splicing, translation, and degradation and their ability to modulate mRNA stability and processing. Understanding RNA modification regulation and its part in the emergence of HCC and NAFLD may provide new avenues for diagnosing and treating these diseases.

Для цитирования: Chen Yuyan, Zhu Zhengyi, Zhang Lu, Wang Jinglin, Ren Haozhen. Roles of N6-methyladenosine epitranscriptome in non-alcoholic fatty liver disease and hepatocellular carcinoma.. Smart medicine. 2023. DOI: 10.1002/smmd.20230008.
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