A decrease of ATP production steered by PEDF in cardiomyocytes with oxygen-glucose deprivation is associated with an AMPK-dependent degradation pathway

We demonstrate a novel mechanism for regulation of cardiac ATP production by PEDF involving AMPKα and PPARγ. PEDF promotes proteasomal degradation of AMPK and, subsequently, reduces ATP production. The reduction of ATP production associated with the decrease of ATP expenditure completed by PEDF increase energy reserves and reduces cell energy failure, prolonging the cell activity during OGD.