Telomeres are fascinating structures found in every cell of our body. Their name comes from the Greek telos (end) and meros (part), which already hints at their function. They are located at the ends of chromosomes and act as true guardians of our genetic information. To better understand them, a common analogy is to imagine chromosomes as shoelaces and telomeres as the plastic caps on the ends that prevent them from fraying and becoming damaged.

Although telomeres do not contain genes or “useful information” in the classical sense, they are repetitive sequences that protect chromosome ends and are essential for DNA to be copied correctly each time a cell divides. The problem is that as the cell divides, telomeres progressively shorten. This happens because, inevitably, DNA replication mechanisms cannot copy the very last fragment at the chromosome ends, a phenomenon known as the “end-replication problem.” As a result, telomeres act as a kind of internal biological clock, since each cell has a limited number of divisions before its telomeres become too short to maintain their protective role. At that point, the cell may enter senescence, a state in which it no longer divides, or it may die. Thus, telomeres are both a safety mechanism and one of the reasons why we are thought to age.

Nevertheless, there is a molecular mechanism to counteract this wear, although it only occurs in certain moments and tissues. It involves an enzyme called telomerase, which can add new DNA repeats to telomeres, extending their length and allowing cells to divide more times than they normally could. For instance, telomerase is very active in cells that need to divide constantly or remain “youthful,” such as germ cells that will give rise to new organisms or embryonic stem cells that generate different tissues during development. In contrast, in most of our adult cells, telomerase is practically inactive, which means telomere shortening continues its natural course.

While telomerase activity is limited to this set of cells, something unexpected happens in cancer: many tumor cells manage to reactivate telomerase, giving them the ability to divide indefinitely. This is one of the reasons why these cells are considered “immortal.” That said, inhibiting telomerase in tumors has been proposed as a therapeutic approach to cancer treatment and is currently under investigation.

Several studies, such as those by Dr. Richard Cawthon and colleagues at the University of Utah, have found a correlation between telomere length and longevity, which supports this hypothesis but is not conclusive. In their study, telomere length explained only about 4% of the differences among the individuals analyzed. Cawthon argues, therefore, that it is not the sole determinant of aging, but rather a phenomenon explained by a combination of physiological, metabolic, and genetic factors. Among them, chronological age—which accounted for 6% of the differences in the study—and oxidative stress stand out. Oxidative stress refers to damage to DNA, proteins, and other molecules caused by oxidants, highly reactive substances produced naturally in the body but also introduced through external agents such as alcohol or tobacco.

Inactivating telomerase could restrict cell division in tumors and, therefore, serve as an adjuvant mechanism alongside other treatments, something already demonstrated in laboratory models. However, the possibility of adverse side effects always exists. Given the crucial importance of this enzyme in other cellular processes, non-specific inhibition could cause complications in fertility, wound healing, and the production of blood and immune system cells.

Figure 1. Telomeres act as cellular timekeepers, gradually shortening with each division and driving the process of aging. Cancer cells, however, bypass this natural limit by reactivating telomerase, achieving indefinite growth and cellular immortality.

But cancer is not the whole story. Telomeres have also been linked to a wide range of age-related diseases, from cardiovascular conditions to degenerative disorders. Moreover, there are rare premature aging syndromes in which telomeres are abnormally short from very early ages, leading to organ failure and a drastic reduction in life expectancy. These observations have turned telomeres into an indicator of cellular health and a biomarker of aging. Some research even suggests that telomere length could help predict the risk of developing certain diseases before clinical symptoms appear.

Scientists are also exploring more optimistic possibilities: could telomerase be reactivated in normal cells to extend their lifespan and combat diseases related to wear and tear? This idea opens the door to regenerative therapies and the potential to delay certain aspects of aging. However, it is a path full of caution, because just as it is risky to over-inhibit telomerase, overstimulating its activity indiscriminately could, ironically, increase the risk of developing cancer. The key lies in finding a balance that allows for cell rejuvenation without triggering uncontrolled proliferation.

The study of telomeres has transformed our understanding of aging. It shows us that the passage of time leaves its mark not only on our external appearance but also on the intimate machinery of our cells. Each division is like a mark on an invisible biological calendar, and telomeres are the hands that indicate how much longer a cell can continue functioning. Learning to interpret that clock and manage it carefully could become one of the greatest revolutions in modern medicine, with applications ranging from oncology to regenerative medicine.

Main reference:

Are telomeres the key to aging and cancer. (s/f). Utah.edu. Recuperado el 26 de septiembre de 2025, de https://learn.genetics.utah.edu/content/basics/telomeres

Other references:

Sansone, V., Le Grazie, M., Roselli, J., Polvani, S., Galli, A., Tovoli, F., & Tarocchi, M. (2020). Telomerase reactivation is associated with hepatobiliary and pancreatic cancers. Hepatobiliary & pancreatic diseases international : HBPD INT, 19(5), 420–428. https://doi.org/10.1016/j.hbpd.2020.04.007

Satyanarayana, A., Manns, M. P., & Rudolph, K. L. (2004). Telomeres and telomerase: a dual role in hepatocarcinogenesis. Hepatology (Baltimore, Md.), 40(2), 276–283. https://doi.org/10.1002/hep.20308

Aubert, G., & Lansdorp, P. M. (2008). Telomeres and aging. Physiological reviews, 88(2), 557–579. https://doi.org/10.1152/physrev.00026.2007