Scientists remove “zombie” cells and reverse liver damage in mice
Killing off “zombie” immune cells may reverse fatty liver disease—and possibly slow aging itself.
Date: April 16, 2026
Source: University of California - Los Angeles Health Sciences
Summary:
A rogue set of “zombie” immune cells may be driving aging and fatty liver disease by flooding tissues with inflammation. Researchers found these cells accumulate with age and high cholesterol—and can make up most of the liver’s immune cells in older mice. When scientists removed them, liver damage was dramatically reversed, even without diet changes.
UCLA scientists have uncovered a harmful group of immune cells that quietly builds up in aging tissues and in the livers of people with fatty liver disease. When these cells were removed in mice, inflammation dropped sharply and liver damage was reversed, even though the animals continued eating an unhealthy diet.
The research, published in Nature Aging, focuses on cellular senescence, a process triggered by stress in which cells stop dividing but do not die. These lingering cells, often called “zombie cells,” remain active in tissues and release a steady stream of inflammatory signals that can damage surrounding cells.
“Senescent cells are fairly rare, but think of them like a broken-down car on the 405,” said Anthony Covarrubias, senior author of the study and a member of the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research at UCLA. “Just one stalled car can back up traffic for miles. Now imagine five or ten of them slowly accumulating. That’s what these cells do to a tissue: even a small number causes enormous disruption.”
Solving the Macrophage Mystery
For years, researchers questioned whether macrophages, the immune cells that patrol the body and clean up debris, could truly become senescent. Many believed they could not. One reason for the confusion is that healthy macrophages already show some of the same molecular features seen in senescent cells, making it difficult to distinguish between normal and dysfunctional states.
The UCLA team addressed this problem by identifying a clear molecular signature. They found that the combination of two proteins, p21 and TREM2, reliably marks macrophages that are truly senescent and no longer functioning properly, while still driving inflammation in nearby tissue.
Using this marker, the researchers observed a dramatic shift with age. In young mice, only about 5% of liver macrophages were senescent. In older mice, that number rose to between 60 and 80%, closely matching the increase in chronic liver inflammation seen with aging.
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