Given that PRKAG2 is the AMPK regulatory subunit, we hypothesize that PRKAG2-AS regulates cardiomyopathy through the transcriptional control of PRKAG2. As a result, our study found that PRKAG2-AS can act as a regulatory element to modulate AMPK activity by regulating the transcription of the PRKAG2 gene and participate in regulating the occurrence of cardiovascular disease. Here, PRKAA2 is linked to cardiovascular disorder.