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Critically short telomeres trigger a DNA damage response and cellular senescence. [32] Mice have much longer telomeres, but a greatly accelerated telomere shortening-rate and greatly reduced lifespan compared to humans and elephants. [33] Telomere shortening is associated with aging, mortality, and aging-related diseases in experimental animals.
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]
This problem makes eukaryotic cells unable to copy the last few bases on the 3' end of the template DNA strand, leading to chromosome—and, therefore, telomere—shortening every S phase. [2] Measurements of telomere lengths across cell types at various ages suggest that this gradual chromosome shortening results in a gradual reduction in ...
Researchers measured the length of each of the participants’ telomeres (protective DNA caps at the ends of chromosomes). Telomeres shorten with age, and the rate of shortening may indicate how ...
Telomere shortening does not occur with age in some postmitotic tissues, such as in the rat brain. [35] In humans, skeletal muscle telomere lengths remain stable from ages 23 –74. [ 36 ] In baboon skeletal muscle, which consists of fully differentiated postmitotic cells, less than 3% of myonuclei contain damaged telomeres and this percentage ...
The typical normal human fetal cell will divide between 50 and 70 times before experiencing senescence. As the cell divides, the telomeres on the ends of chromosomes shorten. The Hayflick limit is the limit on cell replication imposed by the shortening of telomeres with each division. This end stage is known as cellular senescence.
The successive shortening of the chromosomal telomeres with each cell cycle is also believed to limit the number of divisions of the cell, contributing to aging. After sufficient shortening, proteins responsible for maintaining telomere structure, such as TRF2, are displaced, resulting in the telomere being recognized as a site of a double ...
Normal aging is associated with telomere shortening in both humans and mice, and studies on genetically modified animal models suggest causal links between telomere erosion and aging. [10] Leonard Hayflick demonstrated that a normal human fetal cell population will divide between 40 and 60 times in cell culture before entering a senescence phase.