Exploiting the survival wiring of senescent cells
Senescent cells resist death even under stress because they upregulate anti-apoptotic defenses, sometimes called senescent-cell anti-apoptotic pathways (SCAPs). Key nodes include the BCL-2 family of survival proteins and the PI3K/AKT signaling axis, which together keep the cell's self-destruct machinery suppressed.
Senolytics work by interfering with these dependencies. When the propped-up survival signals are removed, the senescent cell, which is already under stress, tips into apoptosis, while normal cells that do not rely as heavily on those defenses are largely spared.
Selectivity and the limits of current evidence
Different senolytics hit different nodes: navitoclax inhibits BCL-2 family proteins, while the dasatinib plus quercetin combination targets several SCAP pathways at once. Because senescent cells vary by tissue and trigger, no single agent clears all of them, which is why combinations and intermittent dosing are studied.
Most supporting data come from cell and animal models; human trials are early-stage, and some agents carry meaningful side effects. This is general educational information about a research area, not medical advice; consult a qualified professional.