Previous evidence has suggested that PARP may be excessively activated by reactive oxygen and nitrogen species in cardiomyocytes and endothelial cells, during myocardial ischemia/reperfusion injury, various forms of heart failure or cardiomyopathies, circulatory shock, cardiovascular aging, diabetic complications, myocardial hypertrophy, atherosclerosis, and vascular remodeling following injury (21). Here, PARP1 is linked to heart failure.