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Cellular Senescence is permanent growth arrest or the irreversible loss in the ability to divide in somatic cells. This serves a practical purpose as it prevents the division of damaged cells.
In the Hallmarks of aging review, the authors state that cellular senescence is brought upon by telomere shortening, non-telomere associated DNA damage and the deactivation of the INK4/ARF inhibitor[1]. These means of causing cellular senescence occur as one ages. Due to the build-up of senescent cells increasing with age it has been hypothesized that cellular senescence is related to aging as the accumulation of the senescent cells may exasperate DNA damage by secreting proinflammatory secretome. The INK4a/ARF locus encodes for the p16INK4a and p53 pathways[1]. These pathways induce senescence and have been linked physiological aging. The authors conclude that cellular senescence is necessary to cells as it halts the division of damaged cells however the accumulation of these senescent cells becomes toxic and accelerates aging.
Much research has been done in the study of cellular senescence since the publication of the Hallmarks of Aging review in 2013. Such research has indicated that cellular senescence may be the driving force behind aging. In a review article titled "Cellular Senescence as the Causal Nexus of Aging" the authors explain that the reason aging is a gradual process because it requires the buildup of senescent cells to show signs of aging. They also indicate that there are various types of damage and stress that can induce cellular senescence [2]. Other research suggests that cellular senescence is the leading cause for age related lung diseases in the elderly [3]. Current research has shown that silencing small GTPase DIRAS3 can affect and induce cellular senescence in adipose stromal/progenitor cells and how this could be a way to control and prevent obesity and thereby extending lifespan [4]. Researchers have also found that MicroRNA-29 can induce cellular senescence in aging muscles and increase the cell arrest proteins like p53, as mentioned in the Hallmarks of Aging review [5].Interestingly resveratrol has also been recently studied as a way to induce cellular senescence in cancer cells and how the effects of RSV could potentially be used as a form of cancer treatment [6]. Whilst many avenues of cellular senescence is being researched, many researchers can agree that it is important to understand cellular senescence and it role on aging to potentially find ways to extend lifespan.
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- ^ a b Lopez-Otin, Carlos; Maria, Blasco; Partridge, Linda; Serrano, Manuel; Kroemer, Guido (2013). "The Hallmarks of Aging". Cell. 153: 1194–1217.
- ^ Bhatia-Dey, Naina; Kanherkar, Riya R; Stair, Susan E.; Makarev, Evgeny O.; Csoka, Antonei B. (12 February 2016). "Cellular Senescence as the Causal Nexus of Aging". Frontiers in Genetics. 7.
- ^ Yanagi, Shigehisa; Tsubouchi, Hironobu; Miura, Ayako; Matsuo, Ayako; Mastumoto, Nobuhiro; Nakazato, Masamistu (25 February 2017). "The Impacts of Cellular Senescence in Elderly Pneumonia and in Age-Related Lung Diseases That Increase the Risk of Respiratory Infections". International Journal of Molecular Sciences. 18.
- ^ Ejaz, Asim; Mattesich, Monika; Zwerschke, Werner (17 March 2017). "Silencing of the Small GTPase DIRAS3 Induces Cellular Senescence in Human White Adipose Stromal/progenitor Cells". Aging. 9.
- ^ Hu, Zhaoyong; Klein, Janet D.; Mitch, William; Zhang, Liping; Martinez, Ivan; Wang, Xioanan H (12 March 2014). "MicroRNA-29 Induces Cellular Senescence in Aging Muscle through Multiple Signaling Pathways". Aging. 6.
- ^ Shao, Changshun; Li, Boxuan; Hou, Dong; Guo, Haiyang; Zhou, Haibin; Jang, SHouji; Xu, Xiuhua; Liu, Qiao; Zhang, Xiyu (15 March 2017). "Resveratrol Sequentially Induces Replication and Oxidative Stresses to Drive P53-CXCR2 Mediated Cellular Senescence in Cancer Cells". Scientific Reports. 7.