Apoptosis, a highly controlled homeostatic mechanism that eliminates single cells without destroying tissue function, occurs during growing development and senescence. N6-methyladenosine (m 6 A), as the most common internal modification of eukaryotic mRNA, fine-tunes gene expression by regulating many aspects of mRNA metabolism, such as splicing, nucleation, stability, translation, and degradation. Remarkably, recent reports have indicated that aberrant methylation of m 6 A-related RNA may directly or indirectly influence the expression of apoptosis-related genes, thus regulating the process of cell apoptosis. In this review, we summarized the relationship between m 6 A modification and cell apoptosis, especially its role in the nervous system, and analyzed the limitations of the current research. Pro-apoptotic protein, anti-apoptotic protein, pro-survival protein, and caspases participate in different processes of apoptosis. METTL3 and METTL14 directly regulate the expression of Bcl-2, Bcl-xl, Bak, Bax, caspase7, caspase3, MYB, and MYC. WTAP, FTO, ALKBH5, YTHDF2, and eIF3 can also control cell apoptosis by regulating the expression of certain genes.
Keyphrases
- cell death
- cell cycle arrest
- binding protein
- induced apoptosis
- endoplasmic reticulum stress
- poor prognosis
- oxidative stress
- gene expression
- cell proliferation
- dna methylation
- genome wide
- anti inflammatory
- transcription factor
- protein protein
- pi k akt
- long non coding rna
- small molecule
- air pollution
- endothelial cells
- stress induced
- free survival