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Hypoxia/ischemia is one of the major causes of mitochondrial dysfunction and neuronal cell death. So far, it has been reported that the DNA damage repair enzyme Poly (ADP-Ribose) Polymerase-1 (PARP1) gets activated during hypoxia/ischemia, leading to mitochondrial membrane permeability transition and caspase independent neuronal death mediated by nuclear translocation of the mitochondrial proapoptotic factor AIF. On the other hand, Bnip3, a proapoptotic BH3-only protein of the Bcl-2 family, is also found to be upregulated during hypoxia/ischemia, resulting in mitochondrial permeability transition and neuronal death in a manner similar to that of PARP1. This led the authors to hypothesize that the pathway of neuronal cell death induced by PARP1 and Bnip3 may be linked. Also, it is reported that PARP1 mediated NAD +  depletion leads to inhibition of SIRT1, a NAD +  dependent class III histone deacetylase enzyme which targets many transcription factors responsible for maintaining mitochondrial integrity including the FoxO (Fork-head box O) family of proteins. Thus, they also hypothesized that PARP1 mediated inhibition of SIRT1 may lead to derepression of FoxO3a resulting in upregulation of Bnip3 under hypoxic conditions.

Poly (ADP-Ribose) Polymerase-1 causes mitochondrial damage and neuron death mediated by Bnip3, J Neurosci. 2014 Nov 26;34(48):15975-87