Parthanatos

Our results suggest that excessive activation of PARP-1 leads to an intrinsic cell death program, which we designate as parthanatos to distinguish from necrosis and apoptosis.

Also, the lack of knowledge of mechanisms of calpain activation in parthanatos makes it difficult to identify calpain as PAR-dependent mediators of AIF release.

The biochemical features of parthanatos are distinct from classically defined pathways of cell death, and include rapid PARP-1 activation, early PAR accumulation, mitochondrial depolarization, early nuclear AIF translocation, loss of cellular NAD and ATP, and late caspase activation.