D heterochromatin formation and silencing of E2F target genes during cellular senescence. Cell 2003, 113:70316. 7. Ben-Porath I, Weinberg RA: The signals and pathways activating cellular senescence. Int J Biochem Cell Biol 2005, 37:96176. eight. Ramsey M, Sharpless N: ROS as a tumour suppressor Nat Cell Biol 2006, 8:1213215. 9. Bartek J, Bartkova J, Lukas J: DNA damage signalling guards against activated oncogenes and tumour progression. Oncogene 2007, 26:7773779. 10. Herbig U, Ferreira M, Condel L, Carey D, Sedivy JM: Cellular senescence in aging primates. Science 2006, 311:1257. 11. Krishnamurthy J, Torrice C, Ramsey M, Kovalev G, Al-Regaiey K, Su L, Sharpless N: Ink4a/Arf expression is a biomarker of aging. J Clin Invest 2004, 114:1299307. 12. Wang C, Jurk D, Maddick M, Nelson G, Martin-Ruiz C, von Zglinicki T: DNA damage response and cellular senescence in tissues of aging mice.Quinidine Aging Cell 2009, eight:31123. 13. Hewitt G, Jurk D, Marques F, Correia-Melo C, Hardy T, Gackowska A, Anderson R, Taschuk M, Mann J, Passos J: Telomeres are favoured targets of a persistent DNA harm response in ageing and stress-induced senescence. Nat Commun 2012, three:708. 14. Jurk D, Wang C, Miwa S, Maddick M, Korolchuk V, Tsolou A, Gonos E, Thrasivoulou C, Saffrey M, Cameron K, von Zglinicki T: Postmitotic neurons develop a p21-dependent senescence-like phenotype driven by a DNA harm response. Aging cell 2012, 11:996004. 15. Sone H, Kagawa Y: Pancreatic beta cell senescence contributes to the pathogenesis of variety two diabetes in high-fat diet-induced diabetic mice. Diabetologia 2005, 48:587. 16. Minamino T, Komuro I: Vascular cell senescence: contribution to atherosclerosis. Circ Res 2007, one hundred:156. 17. Choudhury AR, Ju Z, Djojosubroto MW, Schienke A, Lechel A, Schaetzlein S, Jiang H, Stepczynska A, Wang C, Buer J, Lee HW, von Zglinicki T, Ganser A, Schirmacher P, Nakauchi H, Rudolph KL: Cdkn1a deletion improves stemConclusions Along with its previously documented function as a tumour suppressive mechanism, current evidence strongly implicates cellular senescence in ageing and age-related ailments. Both telomeric and non-telomeric DNA damage has been shown to contribute to the phenotype, with ROS playing an important role in each the induction and stabilisation of senescence. Moreover, the activation of your DDR, along with the MAPK and NF-B pathways has been shown to contribute towards the regulation of each ROS and the SASP.Daidzein In spite of accumulating proof suggesting that ROS and also the SASP cooperate to induce and stabilise the senescent phenotype, additional research is essential to mechanistically delineate their interactions in regulating their response, and their contributions to modulating the surrounding tissue microenvironment.PMID:23291014 Abbreviations DDF: DNA damage foci; DDR: DNA damage response; DSB: double strand break; IFN: interferon; IL: interleukin; NF: nuclear aspect; NHEJ: non-homologous finish joining; p38MAPK: p38 mitogen-activated protein kinase; ROS: reactive oxygen species; SASP: senescence-associated secretory phenotype; TGF: transforming growth factorpeting interests The authors declare that they’ve no competing interests.Correia-Melo et al. Longevity Healthspan 2014, 3:1 http://www.longevityandhealthspan/content/3/1/Page eight of18.19.20.21.22.23.24.25. 26.27.28.29.30.31.32. 33. 34. 35.36.37.38. 39.40.cell function and lifespan of mice with dysfunctional telomeres without the need of accelerating cancer formation. Nat Genet 2007, 39:9905. Rudolph KL, Chang S, Lee HW, Blasco M, Gottlie.
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