Fig. 7: Diagram of the regulatory effect of circDhx32 on cardiac I/R injury.

YTHDF2 and YTHDC1 recognize fewer m6A modification sites on circDhx32 caused by ALKBH5 and increase its stability and nuclear retention in cardiac I/R model mice. Nuclear circDhx32 binds to FOXO1 and then competitively relieves its ability to activate AdipoR1, ultimately inhibiting the expression of AdipoR1 and thereby exacerbating the inflammatory response in cardiac I/R model mice by regulating the AMPK/NF-κB signaling pathway.