Apoptosis is a highly programmed cell death process that can be activated by
various factors and is strictly connected to the pathogenesis of many human diseases,
including neoplastic, neurodegenerative or cardiovascular diseases. Mitochondria play a
key role in the apoptotic process. The permeabilization of the outer mitochondrial
membrane, occurring as mitochondrion is damaged, activates a series of events leading
to cell death. Apoptosis is activated by various factors; among the various hypotheses
formulated, the so-called ‘intrinsic’ pathway theory assumes that the process, which
initiates in the mitochondrion, provokes the release of cytochrome c and other proapoptotic
factors from the mitochondrial intermembrane space to cytosol. In the cytosol,
cytochrome c exerts a pro-apoptotic action binding to the apoptosis protease activation
factor (APAf-1) and forming a complex called ‘apoptosome’. The activation of procaspase
9 initiates an enzymatic reaction cascade leading to cell death. This review
provides an overview of the key role played by mitochondria and cytochrome c in
activating the apoptotic process.
Keywords: Apoptosis, apoptosome, bak, bax, Bcl-2 family proteins, cardiolipin,
cardiolipin peroxidation, caspases, cell death, cyt c peroxidase activity,
Cytochrome c, lipid peroxidation, mitochondria, mitochondrial apoptosis-induced
channel, mitochondrial damage, mitochondrial membrane, neurodegeneration,
permeability transition pore complex, peroxidase activity, reactive oxygen
species.
