We examined the mechanism of neuronal necrosis induced by hypoxia, excitotoxicity or non-excitotoxic hypoxia. Our observations showed that neuronal necrosis can be an active process starting with early mitochondrial swelling, followed by cytochrome c release and caspase cascade. Energy failure and/or calcium overloading of mitochondria may trigger this sequence of events. We called this form of necrosis ‘programmed necrosis’. We discuss in this paper the contribution of another mitochondrial death factor, apoptosis-inducing factor.

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