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| Aging senescence |  | Aging senescence - Cellular senescence - Encyclopedia II |  | | As noted above, senescence is not universal, and senescence is not observed in single celled organisms that reproduce through the process of cellular mitosis. Moreover, cellular senescence is not observed in many organisms, including sponges, corals, and lobsters. In those species where cellular senescence is observed, cells eventually become post-mitotic when they can no longer replicate themselves through the process of cellular mitosis -- i.e., cells experience replicative senescence. How and why some cells become post-mitotic in s ...
|  | | Aging senescence, Aging senescence - Cellular senescence, Aging senescence - Chemical damage, Aging senescence - Evolutionary theories, Aging senescence - Gene regulation, Aging senescence - Miscellaneous, Aging senescence - Neuro-endocrine-immunological theories, Aging senescence - Reliability theory, Aging senescence - Theories of aging, Advanced adult, Ageing, Aging brain, American Aging Association, Biogerontology, Biological immortality, |  | |
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As noted above, senescence is not universal, and senescence is not observed in single celled organisms that reproduce through the process of cellular mitosis. Moreover, cellular senescence is not observed in many organisms, including sponges, corals, and lobsters. In those species where cellular senescence is observed, cells eventually become post-mitotic when they can no longer replicate themselves through the process of cellular mitosis -- i.e., cells experience replicative senescence. How and why some cells become post-mitotic in some species has been the subject of much research and speculation, but (as noted above) it is widely believed that cellular senescence evolved as a way to prevent the onset and spread of cancer. Somatic cells that have divided many times will have accumulated DNA mutations and would therefore be in danger of becoming cancerous if cell division continued.
Lately the role of telomeres in cellular senescence has aroused general interest, especially with a view to the possible genetically adverse effects of cloning. The successive shortening of the chromosomal telomeres with each cell cycle is also believed to limit the number of divisions of the cell, thus contributing to aging. There have, on the other hand, also been reports that cloning could alter the shortening of telomeres. Some cells do not age and are therefore described as being "biologically immortal." It is theorized by some that when it is discovered exactly what allows these cells, whether it be the result of telomere shortening or not, to divide without limit that it will be possible to genetically alter other cells to have the same capability. It is further theorized that it will eventually be possible to genetically engineer all cells in the human body to have this capability by employing gene therapy and thereby stop or reverse ageing, effectively making the entire organism potentially immortal.
Other related archives1968, 1982, Advanced adult, Ageing, Aging brain, American Aging Association, Biogerontology, Biological immortality, Blade Runner, Caenorhabditis elegans, DNA, DNA repair, Dietary calorie restriction, Do Androids Dream of Electric Sheep?, Dolly the sheep,
 Adapted from the Wikipedia article "Cellular senescence", under the G.N U Free Docmentation License. Please also see http://en.wikipedia.org/wiki/Main_Page |
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