Cellular apoptotic pathway

The **cellular apoptotic pathway** encompasses a group of tightly regulated biochemical signaling cascades responsible for programmed cell death (apoptosis) in multicellular organisms. There are two principal and interconnected pathways: - The **intrinsic (mitochondrial) pathway**, activated by internal stress signals such as DNA damage or metabolic dysfunction, relies on proteins from the Bcl-2 family. Pro-apoptotic factors such as BAX and BAK disrupt mitochondrial membrane permeability, leading to the release of cytochrome c and the assembly of the apoptosome (with APAF-1 and caspase-9) and subsequent activation of executioner caspases like caspase-3[1][4][6]. - The **extrinsic (death receptor) pathway** is triggered when extracellular death ligands (such as FasL or TRAIL) bind to their cognate receptors (e.g., Fas/CD95, TRAIL-R1/DR4, TRAIL-R2/DR5), resulting in the recruitment of adaptor proteins and the activation of initiator caspases (notably caspase-8). This pathway may also crosstalk with the intrinsic pathway, amplifying the apoptotic response[3][5][7]. **Cellular apoptotic pathways** are not themselves a single molecular entity but rather comprise multiple molecular targets (including receptors, adaptors, enzymes, and regulatory proteins). Due to defects or dysregulation in these pathways, particularly in cancer and degenerative diseases, therapeutically targeting specific molecules within apoptotic cascades is of significant interest[7][9]. **This entry is not a valid single molecular target but describes a biological process involving many targets; it should be replaced with entries for specific pathway components (e.g., Fas receptor, caspase-3, BAX, Bcl-2, etc.) for structured target databases.**

Other names

Apoptosis pathwayProgrammed cell death pathway