Sex And Stimulus-Specific Differences In Endothelial Cell Senescence Under Hormone-Free Conditions
Our bodies are made of countless cells, and how these cells age can significantly impact our health, especially our cardiovascular system. A process called “senescence” is a key part of aging, where cells stop dividing and can even release substances that harm surrounding tissues. While we know that men and women often experience cardiovascular diseases differently, much of this has been attributed to hormones.
However, new research sheds light on how fundamental biological differences between male and female cells might contribute to these varying aging patterns, even in the absence of hormones. This study focused on endothelial cells, which line our blood vessels and are crucial for heart health. Researchers observed how these cells aged under two different types of stress: normal replication (how many times a cell can divide before stopping) and stress induced by radiation.
Interestingly, the findings revealed a nuanced picture. Female endothelial cells were able to divide more times before showing signs of aging compared to male cells. This suggests that, under normal conditions, female cells might have a longer “replicative lifespan.” However, when exposed to radiation, which mimics a different kind of cellular damage, female cells showed a stronger and earlier senescent response. This means they became senescent more readily under this specific stress.
These results are important because they suggest that intrinsic, non-hormonal factors within male and female cells contribute to how they age and respond to different types of stress. Understanding these “sex- and stimulus-specific mechanisms” in cellular aging could pave the way for more personalized approaches to preventing and treating age-related diseases, including those affecting the heart and blood vessels.
Source: link to paper