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Fig. 4 | Cell & Bioscience

Fig. 4

From: Current insights into the implications of m6A RNA methylation and autophagy interaction in human diseases

Fig. 4

Effects of m6A-autophagy interaction in apoptosis-induced diseases. A Hypoxia/ Reoxygenation (H/R) mediated increased m6A modification could provide stability to TFEB transcripts, promoting autophagy and inhibiting apoptosis of cardiomyocytes. On the contrary, HNRNPD could reduce TFEB mRNA stability which could result in autophagy inhibition and apoptosis induction in cardiomyocytes. B YTHDF2 mediated degradation of FIP200 mRNA causes autophagy inhibition and apoptosis induction in NPCs. BSMCs-NPCs co-culturing could induce autophagy which prevents apoptosis of NPCs

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