Mechanistically, the isoform switch from AMPKα2 to AMPKα1 during HF resulted in the inhibition of PINK1/Parkin/SQSTM1-mediated mitophagy, aggravating mitochondrial dysfunction and severe cardiomyocyte apoptosis via targeting PINK1 dephosphorylation [383]. Here, PRKAA2 is linked to hydrops fetalis.