Sestrins As Biomarkers Of Cellular Stress And Human Disease
Our bodies are constantly working to maintain balance, and when cells experience stress, they activate special proteins to cope. One such family of proteins, known as Sestrins, plays a crucial role in this cellular defense system. These proteins are essential for regulating how our cells use energy (metabolism), maintaining a healthy balance between damaging and protective molecules (redox balance), and ensuring cell survival.
When cells are under duress, for example from oxidative stress (an imbalance leading to cell damage from unstable molecules called reactive oxygen species), Sestrins are produced in greater amounts. This production is controlled by specific “master switch” proteins called transcription factors, such as p53, NRF2, and FOXO, which turn on the genes responsible for making Sestrins.
Once activated, Sestrins act as cellular guardians. They possess antioxidant properties, meaning they help neutralize harmful reactive oxygen species. They also influence key cellular pathways, specifically mTORC1 and mTORC2 signaling, which are like central command systems that regulate cell growth, metabolism, and survival. Furthermore, Sestrins promote a vital cellular “recycling” process called autophagy, where cells break down and remove damaged or unnecessary components to maintain health.
Research shows that the levels of these protective proteins change significantly across many different health conditions, including metabolic disorders, aging-related diseases, heart problems, inflammatory conditions, and neurodegenerative disorders. Interestingly, these changes observed in tissues are often mirrored in the bloodstream. This suggests that by monitoring Sestrin levels in easily accessible samples like blood, we might gain valuable insights into disease progression and how well treatments are working. While Sestrins are not specific to one disease, their dynamic regulation makes them promising candidates as general indicators (biomarkers) of cellular stress and overall disease states.
Source: link to paper