Cellular Senescence Essay

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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
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Figure 4 illustrates these factors and its associated mechanisms (Kaur, 2014). In a study by Ford et al. using the Third National Health and Nutrition Examination Survey (1988-1994), the group estimated an age-adjusted prevalence of metabolic syndrome to be 23.7%. It was estimated that in 2000, 47 million US citizens had metabolic syndrome (Ford, 2002). Because aging has been known to accelerate the predisposing conditions, such as obesity and insulin resistance, which increase metabolic syndrome (Guarner & Maria, 2012), the growing aging population has been an important topic in healthcare and public health (Ford,

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