Abstract
The cellular senescence definition comes to the fact of cells irreversible proliferation disability. Besides the cell cycle arrest, senescent cells go through some morphological, biochemical, and functional changes which are the signs of cellular senescence. The senescent cells (including replicative senescence and stress-induced premature senescence) of all the tissues look alike. They are metabolically active and possess the set of characteristics in vitro and in vivo, which are known as biomarkers of aging and cellular senescence. Among biomarkers of cellular senescence telomere shortening is a rather elegant frequently used biomarker. Validity of telomere shortening as a marker for cellular senescence is based on theoretical and experimental data.
Highlights
Cellular senescence describes how cells can induce an irreversible proliferation disability, which is resistant to growth or proliferation factors [1]
As telomere shortening is related to premature cellular senescence, telomere length may be an effective marker of cellular pathology in neurological diseases; www.impactaging.com it has been demonstrated in dementia, Huntington's disease, and ataxia telangiectasia
The number of β-galactosidase stained cells was found as a function of population doubling level (PDL) on human retinal pigment epithelial cells; while simultaneously telomere length, which was observed in a stage of 12 PDL and in old culture of 57 PDL, shrank from 10 kb to 4kb respectively [73]
Summary
Cellular senescence describes how cells can induce an irreversible proliferation disability, which is resistant to growth or proliferation factors [1]. The single strand tail length varies between approximately 100 and 280 nucleotides in humans [12,13,14,15,16,17] This single strand forms a telomere hairpin loop structure, termed a T-loop, and is often accompanied by numerous proteins, which together works to cap DNA and aid in preventing fusion or damage of the chromosome ends [18,19,20]. The cell cycle arrest is a universal process and starts each time there is a risk of malignization or comes to the final point of cell development – aging This unites the majority of aging theories with mutual pathogenesis
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