Excess PARP-1 activity has been shown to modulate stress related signaling routes and also initiate a caspase independent form of cell death, termed as parthanatos, in the scenario of myocardial ischemia/reperfusion damage [28] doxorubicin induced cardiac injury [29], hyperglycaemia related oxidative damage and endothelial dysfunction [30], acute septic shock [31] and chronic hypertension induced remodeling of rat aorta [32]. Here, PARP1 is linked to endothelial dysfunction.