A team from Osaka University in Japan has discovered that the adaptor protein complex 2 α 1 subunit (AP2A1) can switch cells between youth and aging, marking a crucial step in reversing cellular aging research. The relevant paper was recently published in the journal Cell Signaling. As age increases, senescent cells accumulate continuously in multiple organs of the human body. These cells not only have a significantly larger volume than young cells, but their internal stress fiber tissue has also undergone changes. Scientists have always been puzzled about how aging cells maintain a large 'body size'. Some scientists speculate that this may be because the stress fibers inside aging cells are thicker than those in young cells, and the proteins inside these fibers play a role in supporting aging cells. To validate this hypothesis, the team suppressed the expression of AP2A1 in senescent cells and overexpressed AP2A1 in young cells to observe its impact on aging behavior. The results showed that inhibiting AP2A1 in senescent cells can reverse aging and promote cell regeneration, while overexpression of AP2A1 in young cells accelerates cell aging. In addition, the team found that AP2A1 and integrin β 1 are always inseparable. Integrin β 1 helps cells attach to the surrounding scaffold like collagen matrix proteins. AP2A1 and integrin β 1 move along the enlarged stress fibers inside senescent cells to maintain their large 'body shape'. Given that the expression of AP2A1 is closely related to signs of cellular aging, it has the potential to be used as a biomarker for cellular aging. (New Society)