Apoptotic signaling pathway

The **apoptotic signaling pathway** encompasses the network of molecular signals controlling apoptosis, a regulated process of programmed cell death vital for tissue development, immune function, and the elimination of damaged or dangerous cells[1][4][6]. It comprises two primary arms: - The **intrinsic (mitochondrial) pathway**, regulated by Bcl-2 family proteins and triggered by internal signals such as DNA damage or cellular stress, leading to mitochondrial outer membrane permeabilization and release of cytochrome c, which activates the apoptosome (Apaf-1, cytochrome c, caspase-9) and subsequent executioner caspases[1][7][10]. - The **extrinsic (death receptor) pathway**, activated by external signals (e.g., Fas ligand, TNFα, TRAIL), binding to cell-surface death receptors (Fas, TNF receptor, TRAIL-R1/DR4, TRAIL-R2/DR5), forming the death-inducing signaling complex (DISC) and activating caspase-8 or caspase-10, which in turn activates executioner caspases or cross-talks with the mitochondrial pathway via Bid cleavage[2][3][4][9]. Both pathways converge on the activation of executioner caspases (mainly caspase-3 and caspase-7), resulting in the orderly disassembly and phagocytic removal of dying cells[3][10]. Aberrations in the apoptotic signaling pathway contribute to diseases such as cancer (where apoptosis is inhibited), neurodegenerative diseases (where excessive apoptosis occurs), and immune disorders[3][6]. **Critical Note:** - The **apoptotic signaling pathway** is not a single molecular entity or canonical therapeutic target; rather, it denotes an interconnected set of signaling events and components[1][4]. Drugs target specific molecules within this pathway (e.g., Bcl-2, caspases, death receptors), not the pathway as a whole[5][8]. For structured therapeutic target information, focus on individual molecules such as "Fas receptor (CD95)," "Bcl-2," "Caspase-3," etc.

Other names

Programmed cell death pathwayApoptosis pathwayApoptosis signaling