Researchers at Stanford Medicine tied organ aging to impaired immune clearance by tissue-resident macrophages (TRMs), identifying EP2 signaling as a key control point. In Science, the team reported that TRMs with EP2 intact fail to clear senescent neutrophils as animals age, contributing to organ-wide decline and cognitive impairment. Blocking EP2—either by genetic disruption in TRMs or using an experimental selective EP2 antagonist—preserved youthfulness across multiple organs in mice. The study reframes aging as a clearance failure rather than passive degeneration and points to an actionable drug target in chronic inflammation biology.