Cell death induced by the activity of poly(ADP-ribose) polymerases. DNA damage induced by various stimuli triggers the formation of PAR by PARP-1/-2. Depending on the cell type and the energy capacity, PAR can either directly induce cell death by AIF release or by energy depletion. In this process, necrotic cells release themselves ROS, accelerating the effect. Ischaemia-reperfusion damage acts on the same line. PARP-1 also interacts with NFκB in inflammation processes, which induce cellular NO formation by inducible NO-synthase (iNOS) and accumulation of reactive products. Also, cytokine production and subsequent immune-cell stimulation is under control of NFκB, leading to target cell lysis with release of pro-inflammatory cytokines and death of surrounding cells.

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