Delineation of a Molecular Mechanism for Programmed Cardiac Myocyte Death After Myocardial Infarction
Programmed cardiac myocyte death (apoptosis) increases cardiac damage late after myocardial infarction by extending the infarct and through loss of cardiac myocytes in non-infarcted myocardium. The programmed cell death gene BNip3 was reported by several groups as upregulated in ischemic hearts. We determined the consequences of BNip3 upregulation in mice by forcing its expression through cardiac-specific transgenesis, and by knocking the BNip3 gene out of the mouse genome.