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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]
The role of telomeres and telomerase in cell aging and cancer was established by scientists at biotechnology company Geron with the cloning of the RNA and catalytic components of human telomerase [9] and the development of a polymerase chain reaction (PCR) based assay for telomerase activity called the TRAP assay, which surveys telomerase ...
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.
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]
“I actually did some calculations years ago and found that if we could cure human aging, average human life span would be more than 1,000 years,” he tells Scientific American. “Maximum life ...
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]
Biological immortality (sometimes referred to as bio-indefinite mortality) is a state in which the rate of mortality from senescence (or aging) is stable or decreasing, thus decoupling it from chronological age. Various unicellular and multicellular species, including some vertebrates, achieve this state either throughout their existence or ...
[4] [5] [6] This process is known as "replicative senescence", or the Hayflick limit. Hayflick's discovery of mortal cells paved the path for the discovery and understanding of cellular aging molecular pathways. [7] Cellular senescence can be initiated by a wide variety of stress inducing factors.