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As we grow older, our bodies accumulate "zombie cells"—living cells that have stopped dividing or functioning normally but linger in our tissues, contributing to chronic inflammation and age-related diseases. A new study led by Albert Einstein College of Medicine researchers and published in Nature Aging helps explain why these cells, formally known as senescent cells, become increasingly difficult to eliminate. The research also points to a potential strategy for helping the body rid itself of these cells.

In experiments with mice, the researchers found that declining activity in a cellular recycling process called chaperone-mediated autophagy (CMA) impairs both zombie cells and the immune cells responsible for removing them. Restoring this recycling process reduced senescent-cell buildup and lessened the severity of lung fibrosis, a disease tightly connected to senescence.

"In older animals, age-related changes in both senescent cells and the immune cells responsible for removing them allow these zombie cells to accumulate and play a role in disease," said study leader Ana Maria Cuervo, M.D., Ph.D., distinguished professor of developmental and molecular biology and of medicine, the Robert and Renee Belfer Chair for the Study of Neurodegenerative Diseases and co-director of the Institute for Geroscience at Einstein.

"By restoring cellular recycling, we may be able to help the body's own defenses clear these cells more effectively."

Cuervo is one of the world's leading authorities on CMA, a process that enables the body's cells to remove and recycle damaged or unnecessary proteins.

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