Decreased S100A7 Expression Is Linked To Altered Differentiation-, Autophagy- And Senescence-Related Programs During Skin Aging
Our skin undergoes many changes as we age, leading to wrinkles, dryness, and a loss of elasticity. While we know these changes happen, the exact molecular reasons are still being uncovered. Recent research sheds light on one potential key player: a protein called S100A7, which is naturally found in our skin and helps fight off microbes.
The study found that in older skin cells, specifically the main type of skin cell called keratinocytes, the amount of S100A7 significantly decreases. This reduction isn’t just a passive change; it appears to actively influence several crucial cellular processes.
When S100A7 levels drop, it affects how skin cells mature and specialize (a process called differentiation), how cells clean out damaged components (known as autophagy), and how cells enter a state where they stop dividing and can contribute to aging (called senescence). Essentially, lower S100A7 seems to disrupt the normal functioning of these pathways, accelerating aspects of skin aging.
Interestingly, the researchers observed that by reducing S100A7, they could mimic some of the signs of cellular aging. Conversely, increasing S100A7 levels boosted the cell’s self-cleaning process and reduced these aging-like characteristics. These findings suggest that S100A7 plays a vital role in maintaining healthy skin and its decline contributes to the aging process. Understanding this connection could open doors for new strategies to support skin health as we age.
Source: link to paper