These findings suggest that PRKAG2-AS may contribute to the protection of cardiomyocytes from hypoxia-induced apoptosis or abnormal function by regulating the transcription of PRKAG2b and PRKAG2d. Furthermore, knockdown of PRKAG2 was demonstrated to affect the expression of heart failure markers consistent with the results of PRKAG2-AS knockdown. The gene discussed is PRKAG2; the disease is heart failure.