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How do telomeres influence cellular senescence and apoptosis?

Telomeres gradually shorten with each cell division due to the inability of DNA polymerase to fully replicate the ends of linear chromosomes. This progressive shortening eventually triggers a cellular response known as cellular senescence, which is characterized by irreversible growth arrest.

When telomeres become critically short, they can no longer effectively protect the chromosome ends, leading to the activation of DNA damage response pathways. This activation can induce cellular senescence as a protective mechanism to prevent the propagation of damaged cells that may give rise to cancer.

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In addition to cellular senescence, critically short telomeres can also trigger apoptosis, a programmed cell death process. This occurs when the DNA damage response pathways are unable to repair the telomere dysfunction. Apoptosis helps eliminate cells with dysfunctional telomeres, preventing the accumulation of damaged cells that could potentially lead to genomic instability and tumorigenesis.

Telomere length and function are regulated by various factors, including telomerase, a specialized enzyme that can elongate telomeres by adding repetitive DNA sequences. Telomerase activity is tightly controlled in most somatic cells, resulting in gradual telomere shortening over time.

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Understanding the influence of telomeres on cellular senescence and apoptosis is crucial in the field of longevity research. Manipulating telomere length and function may have implications for extending cellular lifespan and potentially delaying age-related diseases.

Keywords: telomeres, cellular, senescence, apoptosis, telomere, chromosomes, response, influence, repetitive