Blocking a single immune receptor keeps aged mice lean, strong and cognitively sharp
Scientists found that disabling the EP2 receptor on tissue-resident macrophages lets old mice clear senescent neutrophils, preserving youthful organ function and cognition.
Research from Stanford Medicine identified that tissue-resident macrophages lose their capacity to clear senescent neutrophils as organisms age, fueling chronic inflammation. The team demonstrated that the EP2 receptor, which binds the inflammatory hormone PGE2, is central to this decline. Removing EP2 genetically in macrophages, or treating old mice with an experimental EP2 blocker, restored neutrophil clearance and kept inflammatory markers at youthful levels across multiple organs.
Treated mice displayed reduced visceral fat, preserved muscle mass, and performed on cognitive and motor tests comparable to young controls. Analysis of human liver cell databases revealed parallel increases in EP2 activity and neutrophil senescence, suggesting relevance to human aging. The findings point to EP2 inhibition as a promising strategy to slow organ-wide aging and extend healthspan.
Why it matters
Targeting EP2 could lead to therapies that delay age-related decline and chronic diseases.
In this story
