Poly(ADP-ribose) polymerase-1 mediated caspase-independent cell death after ischemia/reperfusion.

摘要: In ischemia/reperfusion (I/R) injury increased intracellular Ca(2+) and production of reactive oxygen species (ROS) may cause cell death by intrinsic apoptotic pathways or necrosis. this review, an alternative pathway, mediated poly(ADP-ribose) polymerase-1 (PARP-1) apoptosis-inducing factor (AIF), is described. ROS-induced DNA strand breaks lead to overactivation the nuclear enzyme (PARP-1; EC 2.4.2.30), causing excessive use energetic substrates such as NAD(+) ATP, inducing either apoptosis Recently, it was demonstrated that activation PARP-1 induces translocation from mitochondria nucleus, condensation fragmentation, subsequent death. This pathway seems be triggered depletion appears caspase independent. Several lines evidence suggest plays a role in I/R injury, although some studies indicate mitochondrial dysfunction also trigger AIF At present, exact mechanisms linking induction are still unclear. Therefore, further investigations will yield valuable information on underlying potential interventions reduce caspase-independent during ischemia-reperfusion.