“Zombie cells” become harder to clear with age, and a new study reveals why the immune system struggles to remove them.

Researchers at Albert Einstein College of Medicine have identified a breakdown in protein recycling that helps explain why senescent cells, often called “zombie cells,” accumulate in aging tissues. In experiments involving older mice, restoring that process reduced senescent-cell buildup, inflammation, and tissue scarring. The findings, published in Nature Aging, suggest a possible way to help the immune system clear these cells more effectively.

Senescent cells remain alive after they stop dividing, but their activity changes. Although they can support tissue repair, their prolonged presence can fuel chronic inflammation and age-related disease. Most of the new experiments involved mice, with human lung samples providing evidence that the biological changes may also occur in people.