Cellular Senescence

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Cellular Senescence

Cellular senescence is an irreversible growth arrest that may be an evolved anti-tumour mechanism. Senescence is a natural mechanism restricting propagation of cells, which passed through genotoxic or oncogene stresses, by epigenetic reprogramming. It is a kind of program or a state, basically subroutine, which the cell adapts after damage, stress or some kind of damaging signal. Senescence is a general purpose mechanism that is used for repair systems. Cellular senescence prevents the proliferation of preneoplastic cells and has beneficial roles in tissue remodelling during embryogenesis and wound healing [Baker+Al:2016]. It is a primitive and very ancient process that even occurs in single cellular organism.

Cellular senescence is induced by short telomeres (replicative senescence), but it can also be induced by various stressors (stress-induced premature senescence). There are more than 50 oncogenic or mitogenic alterations that are able to induce senescence [Gorgoulis+Halazonetis:2010].

There are certain phenotypes associated with the state of cellular senescence such as obvious morphological changes. Senescence cells enlarge and become resistant to apoptosis. Cellular senescence is frequently characterized by the expression of the p16 protein. There is also the formation of senescence-associated heterochromatin foci.

Cellular senescence exhibits a distinctive secretory phenotype [Baker+Al:2016]. This associated secretion profile (Senescence-Associated Secretory Phenotype; SASP) of senescence cells depends on the type of insult. Senescence markers show already up during development. However senescence cells accumulate in various tissues/organs over time [Baker+Al:2016]. It is a growth arrest that for some reason occurs because either the cell is damaged or due to some regenerative response. The type of profile of secretion depends on the context of damage/triggering signalling.

It is commonly believed that cellular senescence underlies organismal senescence in mammals.

[Baker+Al:2016](1, 2, 3) Baker, Darren J; Childs, Bennett G; Durik, Matej; Wijers, Melinde E; Sieben, Cynthia J; Zhong, Jian; Saltness, Rachel A; Jeganathan, Karthik B; Verzosa, Grace Casaclang; Pezeshki, Abdulmohammad; Khazaie, Khashayarsha; Miller, Jordan D; & van Deursen, Jan M (2016). 'Naturally occurring p16(Ink4a)-positive cells shorten healthy lifespan.' Nature. 530(7589), pp. 184-9.
[Gorgoulis+Halazonetis:2010]Gorgoulis, Vassilis G & Halazonetis, Thanos D (2010). 'Oncogene-induced senescence: the bright and dark side of the response.' Current opinion in cell biology. 22(6), pp. 816-27.


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