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Abstract
Telomeres are regions of tandem arrays of TTAGGG repeats and associated proteins located at chromosomal ends that allow cells to distinguish chromosome ends from double-strand breaks and protect chromosomes from end-to-end fusion, recombination, and degradation (Houben et al., 2008). Telomeres are not linear structures, telomeric DNA is maintained in a loop structure due to many key proteins. This structure serves to protect the ends of chromosomes (Neidle and Parkinson, 2003). Telomeres are subjected to shortening at each cycle of cell division due to incomplete synthesis of the lagging strand during DNA replication owing to the inability of DNA polymerase to completely replicate the ends of chromosome DNA (“end-replication problem”) (Muraki et al., 2012). Therefore, they assume to limit the number of cell cycles and act as a “mitotic clock” (Olovnikov, 1996). Shortened telomeres cause decreased proliferative potential, thus triggering senescence (Blackburn et al., 2006).
Highlights
Telomere length (TL) is highly heterogeneous in somatic cells, but generally decreases with age in proliferating tissues thereby constituting a barrier to tumorigenesis and contributing to age-related loss of stem cells
Repair of critically short (“uncapped”) telomeres by telomerase enzyme, which elongates chromosomal ends by synthesizing new telomeric repeats, is limited in somatic cells, and cellular senescence, apoptosis and/or a permanent cell cycle arrest in G1 phase are triggered by a critical accumulation of uncapped telomeres (D’Souza et al, 2013)
Telomere-initiated cellular senescence is a mechanism of eliminating cells with damaged DNA and protection against cancerogenesis, but it may impair the cell function contributing to degenerative organ failure and organismal aging (Chen et al, 2007; Campisi, 2013)
Summary
D.F. Chebotarev Institute of Gerontology, National Academy of Medical Sciences of Ukraine, Kiev, Ukraine Keywords: age-dependent telomere shortening, telomerase, replicative senescence, oxidative stress Telomere-initiated cellular senescence is a mechanism of eliminating cells with damaged DNA and protection against cancerogenesis (through the activation mechanisms of cell cycle arrest or double-strand breaks-induced apoptosis), but it may impair the cell function contributing to degenerative organ failure and organismal aging (Chen et al, 2007; Campisi, 2013).
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