As we get older, our cardiovascular system changes dramatically. Specifically, our blood vessels become stiffer and lose some of their ability to relax. This is known as endothelial dysfunction.
Scientists debate and propose many theories about the specific causes of endothelial dysfunction with aging. Recently, telomeres have become a hot research topic. Telomeres are sequences of DNA that “cap” the ends of chromosomes (think of the end of a shoelace). Each time a cell divides, telomeres shorten. Once telomeres get so short that a cell isn’t able to divide anymore, it becomes what is called senescent, or old. Senescent cells can lead to inflammation and cause damage to surrounding cells, which could lead to unhealthy cardiovascular changes.
This question spurred Samuel Bloom, a PhD student from the University of Utah, to investigate whether telomere uncapping—when telomeres get too short to be able to protect the chromosomes—occurs with age and if this may be one cause of impaired blood vessel health. He presented his research last month at Experimental Biology 2021.
Bloom and his colleagues examined cells from the blood vessels in the lungs from young and old adults to see how age affected telomere uncapping. The study showed that aging does indeed cause telomere uncapping—older adults had 4.5 times more cells containing uncapped telomeres compared to those from the younger people. His lab also found, surprisingly, that mice that were missing a specific telomere protein had stiffer arteries. They also had more signs of cell senescence and their blood vessels didn’t work as well.
Bloom thinks that if we know how senescence occurs, we can identify new ways to prevent it. And that could help delay accelerated aging and prevent people from developing age-associated diseases. He explained that learning about how telomere uncapping promotes cell aging will lead to more research about the risks associated with getting rid of these cells, which have a role in essential physiological processes.
Staying younger may not be as simple as preventing senescence. However, as we learn more about what drives cellular aging, it seems likely that one day we will have better interventions to improve healthspan and lifespan in everyone.
Brady Holmer is a PhD student in exercise physiology at the University of Florida. His lab focuses on cardiovascular physiology, mainly how exercise can play a role in health, disease and aging. Holmer hosts a podcast called “Science & Chill,” where he sits down with scientists in the fields of physiology, biology, health and nutrition to discuss their work. He served as a meeting blogger for the American Physiological Society’s 2021 annual meeting at Experimental Biology.