Stanford Medicine researchers reported in Science that restoring senescent-neutrophil clearance by tissue-resident macrophages can limit organ-wide aging in mice and preserve youth-like function. The study identifies EP2 signaling in tissue-resident macrophages (TRMs) as a central regulator of how aged neutrophils accumulate. Using genetic receptor disruption or an experimental selective EP2 antagonist drug, the team reported preserved clearance of senescent neutrophils and protection across multiple organs, including brain, heart, skeletal and heart muscle, liver, spleen, bone marrow, kidney, and colon. The work reframes aging as a failure of active cellular clearance rather than purely passive degeneration, and it points to EP2 as a druggable entry point for health-span interventions.