Blocking One Immune Signal Reversed Signs of Aging in Mice
"We've been trying to figure out why."
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Researchers at Stanford University have discovered a potential mechanism behind biological aging by studying how the immune system functions in aging mice. The team, whose findings were published in Science, found that as organisms grow older, certain immune cells become less efficient at removing damaged neutrophils—a type of white blood cell. When these aging neutrophils accumulate in tissues, they can trigger chronic inflammation and contribute to organ deterioration.
The scientists identified a receptor called EP2 as a key player in this process. Located on macrophages, cells responsible for cleaning cellular waste, the EP2 receptor becomes increasingly active with age and impairs their ability to clear away senescent neutrophils. When the research team blocked or disabled EP2 signaling in older mice using both pharmaceutical and genetic approaches, the animals showed remarkable improvements. These included restored youthful inflammation patterns, enhanced memory function, increased muscle mass, and better heart performance.
The study revealed that disabling EP2 restored nearly 60 of 71 proteins that had changed during aging, with the liver emerging as a major contributor to these aging-related changes. Significantly, the researchers observed similar patterns in human tissue samples, suggesting the findings may eventually apply beyond mice. However, experts caution that translating these results into human treatments presents substantial challenges, as no currently approved drugs specifically target EP2 in this manner.
Despite these limitations, the research provides crucial insights into aging mechanisms and suggests that drugs targeting this immune pathway could eventually help slow age-related decline in humans.
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Originally reported by Sciencealert →
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