Researchers have discovered a key protein that could reverse aging at the cellular level. Scientists from Osaka University found that the protein subunit called AP2A1 could play a significant role in the unique structural organization of aged cells. It was noted that suppressing AP2A1 reversed aging in cells, while an increase in its expression accelerated the aging process. The lead author of the study, Pirawan Chantachotikul, stated, “We have yet to understand how aged cells maintain their large sizes. An interesting clue is that stress fibers in aged cells are much thicker than in young cells, indicating that the proteins in these fibers help support the large sizes of cells.”

To investigate this possibility, researchers examined AP2A1 (Adaptor Protein Complex 2, Alpha 1 Subunit). AP2A1 is a protein that is increased in stress fibers in aged cells, particularly in fibroblasts and epithelial cells. Scientists studied behaviors similar to aging by eliminating AP2A1 expression in aged cells and overexpressing it in young cells.

Senior author Shinji Deguchi commented, “The results were very intriguing. Suppressing AP2A1 in aged cells promotes cellular renewal by reversing aging, while overexpression of AP2A1 in young cells accelerates aging.” Researchers also found that AP2A1 is closely associated with integrin β1, a protein that helps cells attach to the collagen matrix surrounding them, and both proteins move along stress fibers inside cells. It was reported that integrin β1 strengthens cell-substrate adhesions in fibroblasts, which may explain the thicker or elevated structures of aged cells.

Chantachotikul stated, “Our findings show that aged cells maintain their large sizes through the movement of AP2A1 and integrin β1 along expanded stress fibers, strengthened adhesion to the extracellular matrix.” The research team also suggested that this study could provide a new treatment target for diseases associated with aging.