Fig. (4).

Schematic representation of the caspase-mediated apoptosis. Caspases can be activated by either extrinsic or intrinsic death stimuli. Extrinsic death signals activate the initiator caspases, which in turn induce the effector caspases, promoting the proteolytic cleavage of cellular targets. Intrinsic death stimuli induce mitochondrial damage, resulting in the cytosolic release of cytochrome c that binding to Apaf1, resulting in the activation of initiator caspases and then to the induction of effector caspases and subsequently to cell death.