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The mitochondria-mediated caspase pathway (mitochondrial or intrinsic apoptosis pathway) is a highly conserved cellular process regulating programmed cell death in response to internal cues such as DNA damage, oxidative stress, or loss of survival signals. Central to this pathway is mitochondrial outer membrane permeabilization, governed by interactions between pro- and anti-apoptotic Bcl-2 family proteins. Once permeabilization occurs, cytochrome c and other apoptogenic factors are released into the cytosol, leading to apoptosome formation, activation of initiator caspase-9, and a cascade resulting in cell demolition via effector caspases. The integrity of this pathway is crucial in cancer, neurodegeneration, immune regulation, and tissue homeostasis, with numerous drugs under investigation aimed at modulating its molecular components for therapeutic benefit[1][2][3].
Induction of mitochondrial outer membrane permeabilization; Release of cytochrome c and pro-apoptotic factors; Activation of initiator caspase-9 via apoptosome, and downstream effector caspases (e.g., caspase-3/7); Inhibition of anti-apoptotic Bcl-2 proteins promotes apoptosis
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