Scientists from Osaka University have identified a key protein, AP2A1, that holds the potential to reverse cellular aging. The study found that suppressing AP2A1 in older cells led to rejuvenation, while overexpressing it in young cells accelerated senescence. This protein interacts with integrin β1, which strengthens cell adhesion and contributes to the enlarged structure of aging cells.
Researchers manipulated AP2A1 to determine its effects on cellular behavior. Suppressing AP2A1 in older cells reversed senescence and promoted cellular rejuvenation, while overexpressing it in young cells advanced senescence. The findings provide new insights into how stress fibers influence cell size and senescence. AP2A1 could serve as a biomarker for aging and a target for therapies aimed at slowing down or even reversing the aging process.
The discovery of AP2A1’s role in cellular aging has significant implications for the development of age-related diseases and skin health treatments. As our cells age, fewer active cells accumulate, leading to organ dysfunction. By understanding how AP2A1 regulates cell behavior, researchers may uncover new strategies for combating age-related diseases. The study’s findings also shed light on the relationship between stress fibers and cellular size, offering a promising avenue for future research.
Source: https://neurosciencenews.com/cellular-aging-protein-genetics-28436