Suga, N.; Ikeda, Y.; Yoshikawa, S.; Taniguchi, K.; Sawamura, H.; Matsuda, S. In Search of a Function for the N6-Methyladenosine in Epitranscriptome, Autophagy and Neurodegenerative Diseases. Neurol. Int.2023, 15, 967-979.
Suga, N.; Ikeda, Y.; Yoshikawa, S.; Taniguchi, K.; Sawamura, H.; Matsuda, S. In Search of a Function for the N6-Methyladenosine in Epitranscriptome, Autophagy and Neurodegenerative Diseases. Neurol. Int. 2023, 15, 967-979.
Suga, N.; Ikeda, Y.; Yoshikawa, S.; Taniguchi, K.; Sawamura, H.; Matsuda, S. In Search of a Function for the N6-Methyladenosine in Epitranscriptome, Autophagy and Neurodegenerative Diseases. Neurol. Int.2023, 15, 967-979.
Suga, N.; Ikeda, Y.; Yoshikawa, S.; Taniguchi, K.; Sawamura, H.; Matsuda, S. In Search of a Function for the N6-Methyladenosine in Epitranscriptome, Autophagy and Neurodegenerative Diseases. Neurol. Int. 2023, 15, 967-979.
Abstract
Changes in epitranscriptome with N6‐methyladenine (m6A) modification could be involved in the development of multiple diseases, which might be a prevalent modification of messenger RNAs (mRNAs) in eukaryotes. The m6A modification might be performed through the action of methyltransferases, demethylases, and methylation-binding proteins. Importantly, the m6A methylation may be associated with various neurological disorders including Alzheimer's disease (AD), Parkinson's disease (PD), depression, aging related diseases, and/or aging itself. In addition, the m6A methylation might functionally regulate the eukaryotic transcriptome by influencing splicing, export, subcellular localization, translation, stability, and decay of mRNAs. Neurodegenerative diseases may possess a wide variety of phenotypes depending on the neurons that degenerate at occasions. Interestingly, increasing number of evidences have indicated that m6A modification could modulate the expression of autophagy-related genes and promote autophagy in neuronal cells. Oxidative stresses such as reactive oxygen species (ROS) could stimulate the m6A RNA methylation, which may be also related to the regulation of autophagy and/or the development of neurodegenerative diseases. Both m6A modification and autophagy could also play critical roles in regulating health condition of neurons. Therefore, a comprehensive understanding of the m6A and autophagy relationship in human diseases may benefit in developing therapeutic strategies in the future. This paper reviews advances in the understanding of the regulatory mechanisms of m6A modification in the occurrence and development of neurodegenerative diseases and/or aging, discussing the possible therapeutic procedures related to mechanisms of m6A RNA methylation and autophagy.
Biology and Life Sciences, Neuroscience and Neurology
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