Stanford-affiliated researchers linked organ aging to impaired clearance of senescent neutrophils and identified a key signaling axis involving tissue-resident macrophages and EP2. The study, published in Science, reported that blocking EP2 on tissue-resident macrophages preserved youthfulness across multiple organs in mice. Lead author Katrin Andreasson and first author Jessy Tan described an approach using genetic disabling of EP2 in tissue-resident macrophages or an experimental selective EP2 antagonist drug. Both strategies reduced chronic inflammation-associated disorders, including frailty measures, fat accumulation, cardiac issues, and cognitive decline. The work reframes aging as a clearance failure rather than passive degeneration and points to a potential pharmacologic lever within immunology-driven senescence pathways.