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Telomere dysfunction during cellular aging (a state in which cells do not divide but are metabolically active) affects the health of the body. [2] Preventing telomere shortening without clearing old cells may lead to the accumulation of these cells in the body and contribute to age-related diseases and tissue dysfunction. [29]
Telomere shortening is associated with aging, mortality, and aging-related diseases in experimental animals. [ 8 ] [ 34 ] Although many factors can affect human lifespan, such as smoking, diet, and exercise, as persons approach the upper limit of human life expectancy , longer telomeres may be associated with lifespan.
Two concerns with applying telomerase inhibitors in cancer treatment are that effective treatment requires continuous, long-term drug application and that off-target effects are common. [30] For example, the telomerase inhibitor imetelstat, first proposed in 2003, [31] [32] has been held up in clinical trials due to hematological toxicity. [30]
The lack of telomerase does not affect cell growth until the telomeres are short enough to cause cells to "die or undergo growth arrest". However, inhibiting telomerase alone is not enough to destroy large tumors. It must be combined with surgery, radiation, chemotherapy or immunotherapy. [57]
An enzyme called telomerase elongates telomeres in gametes and stem cells. [12] Telomerase deficiency in humans has been linked to several aging-related diseases related to loss of regenerative capacity of tissues. [13] It has also been shown that premature aging in telomerase-deficient mice is reverted when telomerase is reactivated. [14]
Not only does p16 play an important role in aging, but also in auto-immune diseases like rheumatoid arthritis that progressively lead to mobility impairment in advanced disease. [ 42 ] In the nervous system, senescence has been described in astrocytes and microglia, but is less understood in neurons. [ 22 ]
Telomerase is a ribonucleotide protein that helps repair and replace degraded telomeres. However, telomerase fails us as we age; it becomes less able to repair telomeres, and our whole body starts falling apart. This means that our cells can no longer divide or divide with errors, and some believe that this contributes to the process of aging.
Alternative Lengthening of Telomeres (also known as "ALT") is a telomerase-independent mechanism by which cancer cells avoid the degradation of telomeres.. At each end of the chromosomes of most eukaryotic cells, there is a telomere: a region of repetitive nucleotide sequences which protects the end of the chromosome from deterioration or from fusion with neighboring chromosomes.