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• W4313897744 endingPage "720" @default.
• W4313897744 startingPage "705" @default.
• W4313897744 abstract "Autophagy is an evolutionarily conserved cellular degradation and recycling process. It is important for maintaining vital cellular function and metabolism. Abnormal autophagy activity can cause the development of various diseases. N6-methyladenosine (m6A) methylation is the most prevalent and abundant internal modification in eukaryotes, affecting almost all aspects of RNA metabolism. The process of m6A modification is dynamic and adjustable. Its regulation depends on the regulation of m6A methyltransferases, m6A demethylases, and m6A binding proteins. m6A methylation and autophagy are two crucial and independent cellular events. Recent studies have shown that m6A modification mediates the transcriptional and post-transcriptional regulation of autophagy-related genes, affecting autophagy regulatory networks in multiple diseases. However, the regulatory effects of m6A regulators on autophagy in human diseases are not adequately acknowledged. In the present review, we summarized the latest knowledge of m6A modification in autophagy and elucidated the molecular regulatory mechanisms underlying m6A modification in autophagy regulatory networks. Moreover, we discuss the potentiality of m6A regulators serving as promising predictive biomarkers for human disease diagnosis and targets for therapy. This review will increase our understanding of the relationship between m6A methylation and autophagy, and provide novel insights to specifically target m6A modification in autophagy-associated therapeutic strategies." @default.
• W4313897744 created "2023-01-10" @default.
• W4313897744 creator A5007491100 @default.
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• W4313897744 creator A5017084251 @default.
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• W4313897744 creator A5076699095 @default.
• W4313897744 date "2023-01-01" @default.
• W4313897744 modified "2023-10-18" @default.
• W4313897744 title "Novel Insights into The Roles of N⁶-methyladenosine (m⁶A) Modification and Autophagy in Human Diseases" @default.
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