Cellular apoptosis pathways

Cellular apoptosis pathways encompass highly conserved signaling networks that drive regulated cell death, crucial for development, tissue homeostasis, and immune defense. They are split into the intrinsic pathway, typified by mitochondrial permeabilization and BCL-2 family control, and the extrinsic pathway, initiated by ligand binding to death receptors (such as Fas, TNFR1, DR4, and DR5) and subsequent formation of the death-inducing signaling complex (DISC)[1][3][4][5][6][7]. Both converge on the activation of caspase enzymes, which orchestrate cellular demolition with minimal inflammation. Dysregulation of apoptosis underlies tumorigenesis, resistance to cancer therapy, and a range of degenerative, inflammatory, and infectious diseases[1][2][3][5][6]. Therapeutic targeting focuses on promoting apoptotic signals in cancer cells (by activating death receptors, restoring p53, or inhibiting antiapoptotic proteins) while limiting toxicity in normal tissues[1][2][4][5][6][7]. Note: The term "Cellular apoptosis pathways" refers to biological processes rather than a distinct molecular target; therefore, it is not a therapeutic target per se and is not a correctly specified molecule, receptor, or protein for drug development[1][3][6][7]. Use the death receptors (e.g., TRAIL-R1, DR4) or BCL-2 family members as specific canonical targets for drug discovery.

Other names

apoptosis signaling pathwayprogrammed cell death pathwaycaspase pathwayextrinsic pathway (death receptor mediated)intrinsic pathway (mitochondria mediated)

Induction of death receptor-mediated apoptosis; Activation or mimicry of proapoptotic proteins (TRAIL, FasL); Inhibition of antiapoptotic proteins (IAPs, BCL-2 family); Restoration or activation of p53 function; Activation of caspase cascade (initiator and executioner caspases)