What process is initiated at the mitochondrial level during intrinsic apoptosis?

During intrinsic apoptosis, the key event at the mitochondrial level is the release of cytochrome c. This process is crucial as cytochrome c is a component of the electron transport chain, but in the apoptotic pathway, it plays a pivotal role in activating the apoptosome. When cellular stress occurs, such as DNA damage, oxidative stress, or growth factor withdrawal, pro-apoptotic signals lead to changes in the mitochondrial membrane's permeability.

These changes are mediated by proteins from the Bcl-2 family, where pro-apoptotic members (like Bax or Bak) promote the formation of pores in the mitochondrial membrane. The release of cytochrome c from the mitochondria into the cytosol triggers the formation of the apoptosome, a complex that activates initiator caspases, which then go on to execute the cell death program.

This makes the release of cytochrome c a central event in the intrinsic pathway of apoptosis, leading to the activation of downstream effector caspases and the ultimate dismantling of the cell. Other processes may occur simultaneously during intrinsic apoptosis, but the release of cytochrome c is particularly critical for the signaling cascade that leads to programmed cell death.