Apoptosis induction pathway

**Apoptosis induction pathways** refer to the complex cellular signaling networks that regulate programmed cell death (apoptosis). These are not a single molecule or receptor but rather encompass two main mechanistic routes:\n\n*Intrinsic (mitochondrial) pathway*: Triggered by internal stress signals such as DNA damage, oxidative stress, or growth factor deprivation. This pathway involves activation of pro-apoptotic Bcl2 family proteins (e.g., BAX, BAK), leading to mitochondrial outer membrane permeabilization and release of cytochrome c. Cytochrome c then forms the apoptosome with APAF1 and procaspase 9, activating executioner caspases (3, 6, 7) that dismantle the cell[1][2][4].\n\n*Extrinsic (death receptor) pathway*: Initiated by external ligands binding to death receptors on the cell surface—such as Fas/CD95 or TRAIL receptors—leading to formation of the DISC complex and activation of initiator caspase 8. Caspase 8 can directly activate executioner caspases or amplify apoptosis via BID cleavage and mitochondrial involvement[6][7].\n\nBoth intrinsic and extrinsic pathways converge at effector caspases for final cellular demolition. Dysregulation in these pathways is implicated in cancer development/resistance as well as other diseases[1][5]. Therapeutic strategies often target specific molecules within these cascades rather than "apoptosis induction pathway" itself.\n\nBecause "Apoptosis induction pathways" describes a set of processes—not a discrete molecular entity—it is **not considered a therapeutic target** like an enzyme or receptor; thus this entry is **incorrect as a molecular target** for drug discovery purposes[1][2].

Other names

Apoptotic pathwaysProgrammed cell death pathwaysIntrinsic and extrinsic apoptosis pathways