The Programming Of Systemic Ageing Involving Ikk B, Nf Kb And Gnrh

1453 Words Mar 14th, 2015 null Page
Hypothalamic programming of systemic ageing involving IKK-b, NF-kB and GnRH (Zhang et al., 2013).

Cellular senescence is when a cell’s replicative mechanism becomes arrested. This was phenomenon was first described in Hayflick’s experiment. Cellular senescence is usually due to protect the cell from becoming cancerous but it also plays a prominent role in aging (van Deursen, 2014). While senescence describes a halt in proliferation, cancer development is the uncontrolled proliferation of cells (DePinho, 2000). Although these two phenomenon seem to contradict each other, their causes can mostly be explained by accumulation in cell damage (López-Otín et al., 2013). Cellular senescence is one of the hallmarks of aging. Some important functions of cellular senescence in young cells include tissue homeostasis, but more importantly, they can block proliferation of damaged cells, allowing anti-aging or anti-cancer effects. However, in old cells, cellular senescence can maintain anti-cancer effects but it can also decrease tissue function, in crease inflammation, or exhaust stem cells. These can all contribute to the aging process (López-Otín et al., 2013). Specifically, one example cause of cellular senescence is telomere attrition, which are susceptible to age-related deterioration (Blackburn, Greider, & Szostak, 2006). Because DNA polymerase cannot replicate the terminal end of DNA, the strand becomes shorter after each replication, which ultimately causes senescence…

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