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Einstein Researchers Explain Why Zombie Cells Build Up With Age

Einstein Researchers Explain Why Zombie Cells Build Up With Age
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Researchers at the Albert Einstein College of Medicine have identified that declining cellular recycling, known as chaperone-mediated autophagy, contributes to the accumulation of 'zombie cells' in aging bodies. Restoring this process may help the immune system clear these cells and reduce age-related diseases.

Why it matters

Understanding the mechanisms of cellular aging offers potential therapeutic pathways for treating chronic inflammation and age-related conditions.

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October 5, 2026 - (BRONX, N.Y.) - 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 today 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.

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