Abstract
Autophagy is a conserved degradation process crucial to maintaining the primary function of cellular and organismal metabolism. Impaired autophagy could develop numerous diseases, including cancer, cardiomyopathy, neurodegenerative disorders, and aging. N6-methyladenosine (m6A) is the most common RNA modification in eukaryotic cells, and the fate of m6A modified transcripts is controlled by m6A RNA binding proteins. m6A modification influences mRNA alternative splicing, stability, translation, and subcellular localization. Intriguingly, recent studies show that m6A RNA methylation could alter the expression of essential autophagy-related (ATG) genes and influence the autophagy function. Thus, both m6A modification and autophagy could play a crucial role in the onset and progression of various human diseases. In this review, we summarize the latest studies describing the impact of m6A modification in autophagy regulation and discuss the role of m6A modification-autophagy axis in different human diseases, including obesity, heart disease, azoospermatism or oligospermatism, intervertebral disc degeneration, and cancer. The comprehensive understanding of the m6A modification and autophagy interplay may help in interpreting their impact on human diseases and may aid in devising future therapeutic strategies.
Highlights
Autophagy is an evolutionarily conserved mechanism that widely occurs in eukaryotic organisms
methyltransferase-like 3 (METTL3) mediated m6A modification of transcription factor EB (TFEB) mRNA resulted in its binding to m6A reader protein heterogeneous nuclear ribonucleoprotein D (HNRNPD)
This study showed that m6A could negatively impact autophagy in Leydig cells (LCs) [48]. m6A modification was observed to attenuate ULK1 and TFEB mRNA levels, which resulted in autophagy inhibition in LCs [13, 17]
Summary
Autophagy is an evolutionarily conserved mechanism that widely occurs in eukaryotic organisms. One report showed that the post-transcriptional regulation of Atg1/ULK1 could be altered by m6A RNA modification, resulting in autophagy inhibition [13].
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