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rather, the ‘dependency of iron’ is evidenced by specific iron chelators that inhibit the induction of death by agents that disrupt cellular redox control (e.g
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Pro-apoptotic elements, BCL2 associated X, apoptosis regulator (BAX) and BCL2 antagonist/killer 1 (BAK1), drive processes such as mitochondrial outer membrane permeabilization and the creation of the mitochondrial permeability transition pore (MPTP), thus regulating the formation of pores in the outer mitochondrial membrane [112]
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