A pioneering research team from Korea University has uncovered how cellular aging can spread throughout the body via the bloodstream, opening new avenues for therapies against age-related decline.
Led by Professor Ok Hee Jeon at the Department of Convergence Medicine, the group discovered that a protein called High Mobility Group Box 1 (HMGB1) plays a crucial role in transmitting cellular aging signals to distant tissues.
This protein is part of the senescence-associated secretory phenotype (SASP), a group of molecules secreted by aging cells that promote inflammation and tissue dysfunction.
While it has long been known that senescent cells secrete inflammatory factors that accelerate aging locally, the mechanism behind the systemic spread of aging was unclear—until now.
The researchers found that a specific form of HMGB1, known as reduced HMGB1 (ReHMGB1), circulates in the blood and triggers aging-like changes in remote organs.
In laboratory and animal studies, ReHMGB1—but not its oxidized counterpart—caused senescence-related markers to rise in various human cell types, including skin fibroblasts, kidney cells, and muscle cells.
Mice treated with ReHMGB1 showed signs of tissue aging, such as increased markers p21 and p16, heightened inflammatory factors, and decreased muscle strength.
Importantly, in a model of muscle injury in middle-aged mice, treatment with antibodies that neutralize HMGB1 reduced aging markers and improved muscle repair and physical performance.
These results suggest that blocking extracellular HMGB1 could become a promising strategy to combat aging and restore tissue function.
Published in the high-impact journal Metabolism – Clinical and Experimental, this study marks a major breakthrough in understanding how aging signals travel through the body and offers hope for future anti-aging treatments.
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