Figure 8.

Schematic illustration of ALKBH5‐HDAC4‐FoxO3 axis promoting denervation‐induced muscle atrophy. In denervated muscles, ALKBH5‐mediated m⁶A demethylation stabilized and increased HDAC4 expression. HDAC4 interacted with FoxO3 and inhibited its degradation in a deacetylation‐dependent manner, ultimately leading to an increase in FoxO3 protein levels and transcriptional activities. Targeting ALKBH5 reduced HDAC4 levels, which in turn suppressed FoxO3 signalling activation and prevented denervation‐induced muscle atrophy.