Telomerase is a ribonucleoprotein DNA polymerase complex that maintains telomere length. In the absence of telomerase activity, telomeres progressively shorten. Telomerase activity is absent in most normal human somatic cells because of the lack of expression of TERT; TERC is usually present. Expression of TERT in cells that otherwise lack telomerase activity causes cells to bypass senescence and crisis, and such cells are usually termed “immortalized.”

When telomeres shorten beyond a critical threshold, cells enter replicative senescence, eventually triggering apoptosis. Telomerase, a ribonucleoprotein enzyme complex, counteracts telomere shortening by appending repetitive sequences to chromosome ends. While most somatic cells exhibit low or undetectable telomerase activity, certain cell types—such as germ cells, stem cells, and cancer cells—maintain high telomerase activity to support continuous proliferation.

Telomeres shorten progressively with each round of DNA replication due to the inability of conventional DNA polymerase to completely replicate the chromosome ends, known as the "end-replication problem." The telomerase enzyme counteracts the telomeric DNA loss by de novo addition of telomeric repeats onto chromosomal ends. Germline and stem cells maintain significant levels of telomerase activity to maintain telomere length and can divide almost indefinitely. Critically short telomeres elicit and sustain a persistent DNA damage response leading to permanent growth arrest of cells known as cellular senescence, a hallmark of cellular ageing. The accumulation of senescent cells in tissues and organs contributes to organismal ageing. Thus, the prevention of telomere shortening is a promising means to delay or even reverse cellular ageing.

As a normal cellular process, a small portion of telomeric DNA is lost with each cell division. When telomere length reaches a critical limit, the cell undergoes senescence and/or apoptosis. Telomere length may therefore serve as a biological clock to determine the lifespan of a cell and an organism. Telomerase activity, the ability to add telomeric repeats to the chromosome ends, is present in germline, hematopoietic, stem, and certain other rapidly renewing cells but extremely low or absent in most normal somatic cells. Transgenic induction of a telomerase gene in normal human cells extends their lifespan.

Although telomeres are actively maintained in human germ line cells and embryonic stem cells through the expression of telomerase, telomeres shorten when human somatic cells divide due to insufficient telomerase expression. Approximately 50–200 bp of telomeric repeat sequences are lost each time a mammalian cell divides.

Telomeres shorten after each cell division due to the end replication problem, which is the inability of DNA polymerase to fully replicate the 3' ends of linear chromosomes and exonuclease degradation of the telomeric 5′ strand; telomere length serves as a powerful biomarker of aging and age-related pathological conditions. Typically, telomeres lengthen through telomerase activity.

Repression of telomerase in the somatic tissues of humans, and probably other long-lived mammals, appears to have evolved as a powerful protective barrier against cancer. Immortalization in vitro of normal human cells that lack telomerase involves the reactivation of telomerase or, rarely, an alternative (ALT) mechanism for maintaining telomeres.

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. This catalytic cycle determines the ability of the human telomerase enzyme to synthesize DNA “repeats”... and so afford immortality in cells. However, the activity of telomerase in adult stem cells merely slows down the countdown of the molecular clock and does not completely immortalize these cells. Just as youthful stem cells use telomerase to offset telomere length loss, cancer cells employ telomerase to maintain their aberrant and destructive growth.

A new procedure can quickly and efficiently increase the length of human telomeres, the protective caps on the ends of chromosomes that are linked to aging and disease, according to scientists at the Stanford University School of Medicine. Treated cells behave as if they are much younger than untreated cells, multiplying with abandon in the laboratory dish rather than stagnating or dying.

As cells replicate, telomeres shorten at the end of chromosomes, and this process correlates to senescence or cellular aging. Integral to this process is telomerase, which is an enzyme that repairs telomeres and is present in various cells in the human body, especially during human growth and development. However, too much telomerase can also lead to cancer by helping cells to become functionally immortal by avoiding the Hayflick Limit.

Telomeres act as protective caps at the ends of chromosomes, shortening with each cell division, which is a process intrinsically connected to aging. Their length serves as a biological marker of a cell's age and its remaining lifespan. Telomerase can add length to telomeres, potentially slowing or reversing the aging process. However, heightened telomerase activity is present in approximately 90% of malignant tumors, underscoring its significance in cancer biology. By maintaining telomere length, telomerase grants cancer cells a sort of 'immortality,' enabling them to grow and divide beyond the usual limits that non-cancerous cells face.