The extrinsic and intrinsic routes to cell death
Apoptosis can be triggered by two distinct routes that converge on the same machinery. The extrinsic pathway begins at the cell surface, where death-signal molecules bind death receptors (such as Fas and TNF receptors) and assemble a complex that activates initiator caspases. It is often how immune signals instruct a target cell to self-destruct.
The intrinsic, or mitochondrial, pathway responds to internal stress such as DNA damage, oxidative stress, or growth-factor withdrawal. These signals tip the balance of Bcl-2 family proteins, allowing pore-forming proteins to release cytochrome c from mitochondria, which assembles the apoptosome and activates caspase-9.
Where the pathways meet
Both routes funnel into executioner caspases, especially caspase-3, which carry out the actual dismantling of the cell by cleaving structural and regulatory proteins. The two pathways can also talk to each other, so they are not fully isolated.
Because faulty apoptosis contributes to cancer (too little) and to degenerative conditions (too much), these pathways are heavily studied as drug targets. This is general educational information about cell biology, not medical advice.