Researchers at Stanford University School of Medicine have found that systemic aging is partly linked to the decline of resident macrophages. With age, these immune cells lose their ability to engulf aged neutrophils, whose production increases over time. The accumulating unused cells release toxic substances, triggering chronic inflammation and damaging healthy tissues, reports infohub.kz.
The scientists identified that a key role in this malfunction is played by the EP2 receptor on the surface of macrophages, which responds to the hormone PGE2. As aging progresses, concentrations of PGE2 and EP2 receptors increase, suppressing the macrophages' cleaning function. Blocking this receptor genetically or with an experimental drug in aged mice restored this process. As a result, the animals showed reduced inflammation in the brain, liver, heart, and kidneys, and improved memory, muscle strength, and metabolism.
A parallel analysis of human liver databases confirmed similar changes. Study author Katrine Andreasson notes that developing a selective drug to block EP2 could become a new strategy for slowing age-related diseases in humans. The results were published in the journal Science.