Each time the cell divides, the telomeric DNA shrinks and will eventually fail to secure the chromosome ends. This continuous reduction of telomere length functions as a "molecular clock" that counts down to the end of cell growth. The diminished ability for cells to grow is strongly associated with the aging process, with the reduced cell population directly contributing to weakness, illness, and organ failure.
Counteracting the telomere shrinking process is the enzyme, telomerase, that uniquely holds the key to delaying or even reversing the cellular aging process.
Telomerase offsets cellular aging by lengthening the telomeres, adding back lost DNA repeats to add time onto the molecular clock countdown, effectively extending the lifespan of the cell. However, the activity of the telomerase enzyme is insufficient to completely restore the lost telomeric DNA repeats, nor to stop cellular aging. The activity of telomerase in adult stem cells merely slows down the countdown of the molecular clock and does not completely immortalize these cells.
Therefore, adult stem cells become exhausted in aged individuals due to telomere length shortening that results in increased healing times and organ tissue degradation from inadequate cell populations. Understanding the regulation and limitation of the telomerase enzyme holds the promise of reversing telomere shortening and cellular aging with the potential to extend human lifespan and improve the health and wellness of elderly individuals.
Research from the laboratory of Chen and his colleagues, Yinnan Chen, Joshua Podlevsky and Dhenugen Logeswaran, recently uncovered a crucial step in the telomerase catalytic cycle that limits the ability of telomerase to synthesize telomeric DNA repeats onto chromosome ends. This safe-guarding brake, however, also limits the overall activity of the telomerase enzyme," said Professor Chen.
Moreover, the revelation of the braking system finally solves the decades-old mystery of why a single, specific nucleotide stimulates telomerase activity. By specifically targeting the pause signal that prevents restarting DNA repeat synthesis, telomerase enzymatic function can be supercharged to better stave off telomere length reduction, with the potential to rejuvenate aging human adult stem cells.
This accelerated telomere shortening closely resembles premature aging with increased organ deterioration and a shortened patient lifespan from critically insufficient cell populations. Increasing telomerase activity is the seemingly most promising means of treating these diseases. While increased telomerase activity could bring youth to aging cells and cure premature aging-like diseases, too much of a good thing can be damaging for the individual.
Just as youthful stem cells use telomerase to offset telomere length loss, cancer cells employ telomerase to maintain their aberrant and destructive growth.
Keep reading to learn more about these tiny but important structures and why they could unlock the door to preventing disease and reducing the effects of aging. Your DNA strands become slightly shorter each time a chromosome replicates itself. Telomeres help prevent genes from being lost in this process.
But this means that as your chromosomes replicate, your telomeres shorten. This includes shortening of your telomeres. Telomerase does this by adding additional telomere sequences to the ends of your chromosomes. This means that most of your telomeres continue to get shorter over time. Some people claim that telomere shortening is a major contributor to the aging process and development of disease.
But no one fully understands the impact that telomere shortening has on our overall health. A review suggests that markers indicating DNA damage and decreased telomere function increase with age.
This could be significant: A study found a link between shorter telomeres and an increased rate of death from heart disease and infectious diseases. But this study is nearly 20 years old and only involved participants. More recent meta-analyses also suggest connections between shorter telomeres and coronary heart disease or certain types of cancer. Research into the link between telomere shortening and death is ongoing. Oxidative stress refers to damage to DNA and other biomolecules from reactive oxygen species.
Reactive oxygen species are created by both natural cellular processes within your body and inflammation. You can also acquire them from your environment through things such as pollution, smoking, or alcohol consumption. Over time, the damage to DNA and other biomolecules caused by oxidative stress may contribute to health problems associated with aging.
Read our primer on oxidative stress. The specific cancers associated with shorter telomeres are:. In addition, one of the hallmarks of cancer cells is that they grow and divide rapidly compared to other cells.
So, how do cancer cells not aggressively shorten their telomeres and die off? Telomerase, the enzyme that reduces telomere shortening in certain cells, is reactivated or increased in more than 90 percent of cancers, found a study. But it seems that cancer cells are able to use telomerase to protect their telomeres, delaying their deterioration. Based on this information, some new cancer treatments target telomerase to help destroy cancer cells faster.
Given the links between telomere shortening and disease, some people are now interested in finding ways to lengthen their telomeres. But is this even possible? Morrison Lab. Mukhopadhyay Lab. Munshi Lab. Najafov Lab. Nam Yunsun Lab. Neuromuscular Diseases Laboratory. Neurorepair Lab. Next Generation Sequencing Core. Nicastro Lab. Niederkorn Lab. Nijhawan Lab. Nitschke Lab. Nuclear Magnetic Resonance Lab. Nwariaku Lab. O'Donnell Lab. Otwinowski Lab. Park Lab. Pascual Rare Brain Disorders Lab.
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