A Science study from Stanford Medicine links organ aging to a failure of tissue-resident macrophages to clear senescent neutrophils, identifying EP2 signaling as a central regulator of this process. The paper reports that disabling EP2 on tissue-resident macrophages in mice, or blocking EP2 with an experimental selective antagonist, preserved organ youthfulness across multiple tissues and slowed cognitive decline. Lead author Katrin Andreasson, MD, said the decline does not occur when EP2 is removed or “plugged up by a drug,” positioning EP2 as a potential pharmaceutical lever to restrain systemic inflammation-driven aging-related decline.