Stanford Medicine researchers reported that organ aging is linked to impaired clearance of senescent neutrophils, driven by EP2 signaling in tissue-resident macrophages. In mice and human cells, blocking the EP2 receptor preserved youth-like organ function across multiple tissues and substantially slowed cognitive decline. The work was published in Science (“Restored clearance of senescent neutrophils by tissue-resident macrophages limits organ aging”). Senior author Katrin Andreasson, MD, said EP2 inhibition prevents the organ decline cascade, positioning macrophage-driven clearance failure as a pharmaceutical target rather than passive degeneration.