
Way Aging Spreads Through Your Body Revealed
Based on facts, either observed and verified firsthand by the reporter, or reported and verified from knowledgeable sources.
Newsweek AI is in beta. Translations may contain inaccuracies—please refer to the original content.
For the first time in the world, a Korean research team has discovered how aging in one part of the body can spread to another via the bloodstream.
The discovery offers new insights into how aging works and could lead to treatments that slow—or even reverse—age-related decline in the future.
In their study, professor Ok Hee Jeon and colleagues at Korea University studied on a protein called High Mobility Group Box 1 (HMGB1.)
This protein is released by aging cells and is part of a group of molecules collectively called SASP—short for senescence-associated secretory phenotype.
These molecules are chemical signals that aged, or "senescent," cells use to communicate. They can influence nearby cells—and, in the case of one form of HMGB1, can cause neighboring healthy cells to begin aging as well.
A graphical abstract showing that blocking HMGB1 in mice can reduce this chain reaction and limit the spread of aging cells.'
A graphical abstract showing that blocking HMGB1 in mice can reduce this chain reaction and limit the spread of aging cells.'
Korea University Medicine
Aging Spreads Through the Bloodstream
Until now, it was believed that aging cells only affected their immediate surroundings.
However, the new study shows that aging signals can travel through the bloodstream and impact cells in completely different parts of the body. In other words, aging might spread like a ripple effect across tissues.
The research, published in the journal Metabolism – Clinical and Experimental, identified a special form of HMGB1 called reduced HMGB1 (ReHMGB1).
This form moves through the blood and can cause aging in distant tissues like muscles, kidneys, and skin.
Lab and Animal Testing Show Strong Results
The team tested their theory using both lab-grown cells and live mice. They found that ReHMGB1—but not its oxidized version—triggered aging in several types of human cells. Mice injected with ReHMGB1 showed increased aging markers and experienced muscle weakness.
To dig deeper, researchers studied mice with muscle injuries. When these mice were treated with antibodies that blocked HMGB1, they healed faster, showed fewer signs of aging, and regained strength more effectively.
"This study reveals that aging signals are not confined to individual cells but can be systemically transmitted via the blood," said Professor Jeon.
Do you have a tip on a health story that Newsweek should be covering? Do you have a question about aging? Let us know via health@newsweek.com.
Reference
Shin, J.-W., Jang, D.-H., Kim, S. Y., Lee, J.-J., Gil, T.-H., Shim, E., Kim, J. Y., Kim, H. S., Conboy, M. J., Conboy, I. M., Wiley, C. D., Shin, J.-S., & Jeon, O. H. (2025). Propagation of senescent phenotypes by extracellular HMGB1 is dependent on its redox state. Metabolism - Clinical and Experimental, 168. https://doi.org/10.1016/j.metabol.2025.156259
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