replicative senescence


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replicative senescence

a limitation in the number of times that cells can divide; appears to be a basic feature of somatic cells except for most tumor cells and possibly some stem cells. The cell division s counting mechanism is posited to exist as a consequence of a telomere-shortening hypothesis.

senescence

(se-nes'ens) [L. senescens, growing old]
1. The process of growing old.
2. The period of old age.

premature senescence

Aging (typically of cells, but also of whole organisms) that occurs much earlier than is expected under healthy or optimal conditions.

replicative senescence

Hayflick's limit.
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References in periodicals archive ?
Many gerontologists are studying how silencing and other mechanisms such as telomere shortening influence replicative senescence.
Moreover, most cells in the body do not divide, so in their case, replicative senescence is not a likely cause of aging.
Similarly, SIRT4 and ROS are upregulated during replicative senescence and in response to DNA damage [144, 145]; however, one study shows that SIRT4 depletion reduces ROS [144] and therefore suggests that inhibiting SIRT4 may be a strategy to prevent oxidative stress in MSCs, while another believes that SIRT4 is required for appropriate recovery from cellular stresses [145].
Seluanov, "Sirtuin 6 (SIRT6) rescues the decline of homologous recombination repair during replicative senescence," Proceedings of the National Academy of Sciences of the United States of America, vol.
Friguet, "Protein modification and replicative senescence of WI-38 human embryonic fibroblasts," Aging Cell, vol.
The mitochondrial lncRNA ASncmtRNA-2 is induced in aging and replicative senescence in Endothelial Cells," Journal of Molecular and Cellular Cardiology, vol.
Minet and Gaster [32] demonstrated that replicative senescence results in decreased mitochondrial mass and ATP content in myotubes while mitochondrial ATP synthesis rate normalized to mitochondrial protein was unchanged.
Our data presents that the activity of AK decreased significantly during replicative senescence of myoblasts, which has not been shown before.
Research on the effects of telomerase on Werner syndrome cells was conducted by scientists at Geron and published in the April issue of the FASEB Journal in a paper entitled "Telomerase expression prevents replicative senescence but does not fully reset mRNA expression patterns in Werner syndrome cell strains.
Recent experiments have shown that cell transfection with oligonucleotides identical to the mammalian telomeric repeating sequence, 5'-d(TTAGGG)-3', increases the replicative capacity of a variety of phenotypically normal cell types, consistent with the "telomere hypothesis" to explain replicative senescence.
Replicative senescence has also previously been implicated in atherosclerosis, an age-related cardiovascular disease," stated Dr.