Apoptosis and necrosis represent two fundamentally distinct mechanisms of cell death with profoundly different implications for tissue homeostasis, disease pathogenesis, and clinical management. Apoptosis is programmed cell death—an energy-dependent, genetically regulated process that eliminates damaged, senescent, or unnecessary cells without provoking inflammation. It proceeds through two major pathways: the intrinsic (mitochondrial) pathway, triggered by intracellular stress signals (DNA damage, oxidative stress, growth factor withdrawal) that shift the balance of BCL-2 family proteins toward pro-apoptotic members (BAX, BAK), causing mitochondrial outer membrane permeabilization (MOMP), cytochrome c release into the cytosol, apoptosome formation with APAF-1, and sequential activation of initiator caspase-9 followed by executioner caspases-3, -6, and -7; and the extrinsic (death receptor) pathway, initiated by extracellular ligands (FasL, TNF, TRAIL) binding death receptors (Fas/CD95, TNFR1, DR4/DR5), recruiting FADD adaptor protein and activating caspase-8, which then directly activates executioner caspases or amplifies the signal through the intrinsic pathway via BID cleavage. Executioner caspases systematically dismantle the cell by cleaving structural proteins (lamin, cytoskeletal components), activating DNases (CAD/DFF40) that fragment DNA into characteristic 180-bp nucleosomal ladder patterns, and exposing phosphatidylserine on the outer...