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Fig. 9 | Clinical Epigenetics

Fig. 9

From: Abnormal expression of PRKAG2-AS results in dysfunction of cardiomyocytes through regulating PRKAG2 transcription by interacting with PPARG

Fig. 9

Proper expression of PRKAG2-AS is essential for maintaining heart function. PRKAG2-AS is down-regulated in cardiac ischemia and up-regulated in DCM. PRKAG2-AS interacts with the RBFOX2-PRARG complex to recruit Pol II to the promoter of PRKAG2, promoting transcription of PRKAG2b or PRKAG2d in cardiomyocytes. Aberrant expression of PRKAG2b or PRKAG2d alters AMPK activity, leading to apoptosis and hypertrophy of cardiomyocytes. Up-regulation of PRKAG2b or PRKAG2d in heart failure results in abnormal expression of heart failure markers. Therefore, aberrant expression of PRKAG2-AS induced by hypoxia or other stressors leads to dysfunction of cardiomyocytes, including death and hypertrophy

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