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Apoptosis signaling pathways" refers to a collective network of molecular mechanisms that mediate programmed cell death, an essential process for maintaining tissue homeostasis and eliminating damaged or unnecessary cells[1][3][4][7]. The two main pathways are the intrinsic (mitochondrial) and extrinsic (death receptor-mediated) pathways. The intrinsic pathway is regulated by Bcl-2 family proteins and controlled by mitochondrial outer membrane permeabilization, leading to caspase activation via cytochrome c release[3][6]. The extrinsic pathway is initiated by the binding of extracellular ligands (such as Fas ligand or TRAIL) to their respective death receptors (e.g., Fas/CD95, TRAIL-R, TNFR1/TNFRSF1A), resulting in recruitment of adaptor proteins and activation of initiator caspases (caspase-8, caspase-10)[4][6][10]. Dysregulation of apoptosis signaling pathways is implicated in the pathogenesis of numerous diseases, notably cancer (resistance to apoptosis), neurodegeneration (excessive apoptosis), and autoimmune disorders (defective clearance of cells)[2][5][8]. Therapeutic agents have been developed to target specific molecules within these pathways, but "apoptosis signaling pathways" itself is not a single molecular target.
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