Scientists at Stanford Medicine have identified a potential mechanism underlying the aging process through research conducted in mice and human cells. The study centers on tissue-resident macrophages, specialized immune cells that permanently reside in organs and are responsible for removing dysfunctional cells. The researchers discovered that with advancing age, these macrophages become progressively less effective at clearing senescent neutrophils—white blood cells that have entered a dysfunctional state and accumulate harmful inflammatory substances.
The aging-related decline in macrophage function involves a hormone called PGE2 and its receptor EP2. As animals grow older, PGE2 levels increase while macrophages develop higher concentrations of EP2 receptors. This creates a harmful cycle in which PGE2 repeatedly stimulates EP2 on the macrophages, weakening their ability to engulf and remove senescent neutrophils. The accumulation of these dysfunctional cells then drives chronic, body-wide inflammation associated with aging. The findings appear in a paper published in Science, led by Katrin Andreasson at Stanford Medicine.
When researchers experimentally blocked the EP2 receptor specifically on tissue-resident macrophages in mice, the animals retained more youthful characteristics across multiple organs including the brain, heart, liver, and kidney. The intervention also protected mice from age-related problems including cognitive decline, frailty, excess fat accumulation, and heart dysfunction. These results suggest that a single molecular switch may coordinate aging across diverse tissues and organs throughout the body.
The research points toward potential therapeutic applications. By targeting the EP2 receptor with drugs, it may be possible to restore macrophage function and reduce chronic inflammation in aging individuals. Such an approach could potentially slow age-related deterioration and extend the period during which people maintain good health. The findings provide new insight into how chronic inflammation contributes to the aging process and its associated health consequences.
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