In short
Apoptosis is a tightly regulated form of programmed cell death in which a cell activates its own controlled disassembly, allowing damaged or unneeded cells to be removed without triggering inflammation.
Apoptosis proceeds through an ordered sequence: the cell shrinks, its DNA fragments, its membrane blebs, and the resulting fragments are packaged into apoptotic bodies that are cleared by neighboring cells or immune phagocytes — all without releasing cellular contents into surrounding tissue. This is what distinguishes apoptosis from necrosis, an uncontrolled cell death that spills cellular contents and provokes inflammation.
Two main pathways trigger apoptosis: the intrinsic (mitochondrial) pathway, activated by internal stress signals like DNA damage or oxidative stress and mediated by proteins in the Bcl-2 family and caspases; and the extrinsic pathway, triggered by external signals binding death receptors on the cell surface. Apoptosis is essential during development (sculpting tissues by removing excess cells) and throughout life as a safeguard against cells with damage too severe to repair.
Apoptosis relates directly to cellular senescence: a cell with DNA damage can either undergo apoptosis (removed entirely) or senescence (survives but stops dividing), and which path is taken depends on the cell type, damage severity, and signaling context. Senolytic drugs work by selectively pushing senescent cells — which have often evolved apoptosis-resistance as part of the senescent phenotype — over the threshold into apoptosis, which is the core mechanism behind compounds like the dasatinib-plus-quercetin combination.