The research provides valuable insight on a more serious version of a condition experienced by nearly a quarter of Americans.
If you’ve heard your doctor talk about “fatty liver,” you might imagine it as simply excess fat accumulating in or around the liver. But, fatty liver disease, now more commonly known as steatotic liver disease, is actually one of the most common chronic liver conditions. Nearly 24% of Americans currently have a form called metabolic dysfunction-associated steatotic liver disease (MASLD), according to the American Liver Foundation.
Of those, some go on to develop a more severe form called metabolic dysfunction-associated steatohepatitis (MASH) that causes liver inflammation and damage alongside fat on the liver. However, scientists may have recently discovered why some people progress from fat buildup to the more severe form of liver disease—and the surprising culprit might be the very cells in your body that refuse to die.
In a study published in the journal Nature Communications in December 2025, Mayo Clinic researchers with expertise in hepatology, physiology, and biomedical engineering discovered how so-called “zombie cells”—old cells that have stopped dividing but refuse to vanish—may spark chronic inflammation that worsens MASH, rates of which are projected to increase—and it’s already a leading reason for liver transplantation, according to the Mayo Clinic.
The research team found that the “zombie cells,” technically known as aged or senescent cells, can leak fragments of mitochondrial RNA—the genetic material from the cell’s energy factories—into the cell’s main compartment. From there, the leaked RNA can “mistakenly activate” antiviral sensors known as RIG-I and MDA5, prompting inflammation that can damage nearby tissue.
But, when the researchers blocked the antiviral sensors in lab models, inflammation dropped—and liver tissue looked healthier. They also found that certain proteins, known as BAX and BAK, are gateways that allow mitochondrial RNA to leak in the first place—and the team also looked into how to better inhibit those abilities.
The researchers noted that although there is some research around removing these types of cells, this study focused on how to “quiet” them instead.
“With age, we accumulate ‘zombie’ cells, which can lead to more disease,” says João Passos, PhD, senior author of the study. “Our idea is that if we can quiet these cells earlier, we can prevent runaway inflammation and the development of many age‑related conditions, including liver disease.” He adds that this knowledge allows researchers “to target and delay those processes—potentially benefiting more than one condition.”
MASLD typically affects people who have excess weight, obesity, or metabolic conditions like type 2 diabetes or high blood pressure, according to the Mayo Clinic. MASLD sometimes causes very few symptoms, and when it does, it’s usually fatigue or just general feelings of malaise, and possibly pain in the upper right belly area. If the disease progresses to MASH, symptoms can include itchy skin, abdominal swelling, shortness of breath, swelling of the legs, spider veins, enlarged spleen, change in color on the palms, and yellowing of the skin and eyes.
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