Senescent Cells Are Essentially Cells

Senescent cells are essentially cells that "promote the aging of tissues" (Wade 2011). These cells increase the signs and process of aging within older tissue because they accumulate aging within the skin. They do so by creating a low level of inflammation by increasing the reaction f the immune system within the skin in question. Chambers et al. showed that there is a possibility for homeostasis living systems to not strive for homeostasis.

Essentially, there are certain cells that do not contribute the regulation of the internal environment within the body, and actually disrupt its normal functioning as in the case of cancer cells (Conti 2008). Many types of cells, including undifferentiated stem cells, often do not turn towards promoting homeostasis. This often increases with age. Studies on various forms of progeria show that there are often genetic conditions which can mimic the signs of aging. Huntington-Gilford progeria and Werner's syndrome are dominant genetic diseases that increased the speed of the aging process.

These conditions show that normal aging may be linked to genetic predispositions, as it is triggered by genetic material. 4. Gene splicing alters with age, which means that the process of gene splicing changes with age to trigger the signs and conditions of aging. The quote shows that Hutchinson-Gilford porgeria syndrome is comparable to artificially made senescent cells (Science Daily 2011).

The fact that progeria might be considered a process of normal aging is representative of theses that show the production of progeria as a biomarker of normal cellular aging which can be linked to terminal differentiation (McClintock et al. 2007). 5. There are a number of major causes of aging within the human body. Yet, the Programmed Cellular Aging Theory shows that the biggest causes are actually an impairment of the cell's ability to transfer necessary RNAs.

This is often caused by DNA increasingly turning off particular functions based on a predetermined genetic setting. 6. Aging research must receive more attention within the public eye in order to generate enough funding to really examine the process of aging on a cellular level. It is important to direct future efforts to understanding how the cellular process impacts aging and how it can lead to future developments in preventing aging. 7. Luckily, living organisms can repair damage at the cellular level.

DNA repair and other cellular repair can occur in a number of instances. When DNA is damaged, cells can react through cell cycle checkpoints which allows repair to begin before further division can occur. There is also the prokaryotic SOS response which changes gene expression in bacteria as a result of DNA damage. This response is regulated by the production of certain proteins. Moreover, eukaryotic cells also react to DNA damage through producing proteins that begin the process of DNA repair. 8.

Mice are often the favored mammalian in the testing of aging interventions. This is often because of the fact that there are many mice easily available for testing but also the fact that "generation time is short" (Yuan et al. 2011). Essentially, the aging process and testing in interventions can be done on a much shorter time scale then with tests using monkeys. 9. Enzymes may change the transcription patterns of a cell by adding chemical groups to histone proteins. This process increases the sensitivity to DNase I digestion. 10.

Old stem and progenitor cells in a young systemic environment can be rejuvenated. Heterochronic parabiosis can be restored through the activation of Notch signaling and a "regenerative capacity of aged satellite cells" (Conboy et al. 2005). References Books. W.R. Clark. (2009). Human genetic diseases that mimic the aging process. Progeria? The Progeria Project Foundation. Web. http://www.progeriaproject.com/progeria/mimic.htm Conboy, I.M., Conboy, M.J., Wagers,.