Search results
Results from the WOW.Com Content Network
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.
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.
This means that our cells can no longer divide or divide with errors, and some believe that this contributes to the process of aging. New research has also shown that there is an association between telomere shortening and mitochondrial dysfunction. [33] Nevertheless, over-expression of telomerase increases the chances of cancer.
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 ...
The existence of a compensatory mechanism for telomere shortening was first found by Soviet biologist Alexey Olovnikov in 1973, [4] who also suggested the telomere hypothesis of aging and the telomere's connections to cancer and perhaps some neurodegenerative diseases.
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.
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 ...