The key to reversing cellular aging may lie in a protein responsible for toggling cells between a "young" and an "old" state.

This is the conclusion of researchers from the University of Osaka, who experimented with the expression of the protein "AP2A1" in cells of different ages.

"The results were very intriguing," bioengineering professor Shinji Deguchi, one of the paper's authors, said in a statement.

"Suppressing AP2A1 in older cells reversed senescence [aging] and promoted cellular rejuvenation, while AP2A1 overexpression in young cells advanced senescence," he added.

As we grow in years, older and less active cells begin to accumulate across multiple organs.

These "senescent" cells are both significantly larger than their younger counterparts and have a different configuration of stress fibers -- the structural parts of cells that help them move and interact with their surroundings.

"We still don't understand how these senescent cells can maintain their huge size," said lead study author and bioengineer Pirawan Chantachotikul.

"One intriguing clue is that stress fibers are much thicker in senescent cells than in young cells, suggesting that proteins within these fibers help support their size," she added.

To explore this possibility in their study, the researchers focused on the AP2A1 protein, which is known to be produced in greater quantities in the stress fibers of senescent cells.

The team cultivated human fibroblasts (specialized cells that maintain the structural integrity of tissues) and epithelial cells (which cover the inside and outside surfaces of the body, including skin) in the laboratory.

They then prevented the creation of AP2A1 in older cells and overexpressed the protein in younger cells to see the effects that might have on aging-related behaviors.

The team found that AP2A1 appeared to be involved in toggling cells between their "young" and "old" states -- as senescent cells were rejuvenated by the protein's suppression, while younger cells were aged by its overexpression.

The researchers also discovered that the AP2A1 was often closely associated with another protein: integrin β1, which helps cells attach themselves to the scaffold of collagen that surrounds them. Both proteins, the team explained, move along stress fibers within cells.

Moreover, integrin β1 is seen to strengthen cell-substrate adhesions in fibroblasts, potentially offering an explanation for the thicker stress fibers seen in older cells.

"Our findings suggest that senescent cells maintain their large size through improved adhesion to the extracellular matrix via AP2A1 and integrin β1 movement along enlarged stress fibers," Chantachotikul said.

The link between AP2A1 and senescent cells, the researchers said, means the protein has the potential to be used as a marker for cellular aging.

The team also believes that the findings may offer a new target for future treatments of age-related diseases.

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Chantachotikul, P., Liu, S., Furukawa, K., & Deguchi, S. (2025). AP2A1 modulates cell states between senescence and rejuvenation. Cellular Signalling, 127. https://doi.org/10.1016/j.cellsig.2025.111616