The molecular genetics of cellular senescence in the context of organismal aging
Authors:
Matthew Lacey; Martin Mistrík
Authors‘ workplace:
Ústav molekulární a translační medicíny LF UP a FN Olomouc
Published in:
Čas. Lék. čes. 2020; 159: 88-92
Category:
Review Article
Overview
Cellular senescence is a physiological state generally defined as a stable arrest of proliferation by preventing the cells from cycling. Unlike terminally differentiated cells, that also do not show proliferative activity, cellular senescence is stress induced and blocks the proliferation of cells with theoretical ability to divide (such as progenitor, stem or cancer cells) due to the activity of specific signaling pathways. The number of senescent cells increases during the ontogenesis of an organism. Senescent cells are not only associated with aging, but also significantly influence this process – a fact that is becoming increasingly well documented.
Keywords:
aging – cellular senescence – progeria – Werner syndrome – Cockayne syndrome – ataxia telangiectasia
Sources
- Gurău F, Baldoni S, Prattichizzo F et al. Anti-senescence compounds: A potential nutraceutical approach to healthy aging. Ageing Res Rev 2018; 46: 14–31.
- Franceschi C, Garagnani P, Morsiani C et al. The continuum of aging and age-related diseases: common mechanisms but different rates. Front Med 2018; 5: 61.
- McHugh D, Gil J. Senescence and aging: causes, consequences, and therapeutic avenues. J Cell Biol 2018; 217(1): 65–77.
- He S, Sharpless NE. Senescence in health and disease. Cell 2017; 169(6): 1000–1011.
- Bártková J, Hořejší Z, Koed K et al. DNA damage response as a candidate anti-cancer barrier in early human tumorigenesis. Nature 2005; 434(7035): 864–870.
- Coppé JP, Desprez PY, Krtolica A et al. The senescence-associated secretory phenotype: the dark side of tumor suppression. Ann Rev Pathol 2010; 5: 99–118.
- Watanabe S, Kawamoto S, Ohtani N et al. Impact of senescence-associated secretory phenotype and its potential as a therapeutic target for senescence-associated diseases. Cancer Sci 2017; 108 (4): 563–569.
- Rodier F, Campisi J. Four faces of cellular senescence. J Cell Biol 2011; 192(4): 547–556.
- de Magalhães JP, Passos JF. Stress, cell senescence and organismal ageing. Mech Ageing Dev 2018; 170: 2–9.
- Ogrodnik M, Miwa S, Tchkonia T et al. Cellular senescence drives age-dependent hepatic steatosis. Nat Commun 2017; 8: 15691.
- Freund A, Orjalo AV, Desprez PY et al. Inflammatory networks during cellular senescence: causes and consequences. Trends Mol Med 2010; 16(5): 238–246.
- Xia S, Zhang X, Zheng S et al. An update on inflamm-aging: Mechanisms, prevention, and treatment. J Immunol Res 2016; 2016: 8426874.
- Childs BG, Gluscevic M, Baker DJ et al. Senescent cells: an emerging target for diseases of ageing. Nat Rev Drug Discov 2017; 16(10): 718–735.
- Baker DJ, Petersen RC. Cellular senescence in brain aging and neurodegenerative diseases: evidence and perspectives. J Clin Investig 2018; 128(4): 1208–1216.
- Jaul E, Barron J. Age-related diseases and clinical and public health implications for the 85 years old and over population. Front Public Health 2017; 5: 335.
- Chang J, Wang Y, Shao L et al. Clearance of senescent cells by ABT263 rejuvenates aged hematopoietic stem cells in mice. Nat Med 2016; 22(1): 78–83.
- Košař M, Bártková J, Hubáčková S et al. Senescence-associated heterochromatin foci are dispensable for cellular senescence, occur in a cell type- and insult-dependent manner and follow expression of p16(ink4a). Cell Cycle 2011; 10(3): 457–468.
- Brooks CL, Gu W. The impact of acetylation and deacetylation on the p53 pathway. Protein Cell 2011; 2(6): 456–462.
- Hayflick L. The limited in vitro lifetime of human diploid cell strains. Exp Cell Res 1965; 37(3): 614–636.
- Blackburn EH. Structure and function of telomeres. Nature 1991; 350(6319): 579–573.
- Fumagalli M, Rossiello F, Clerici M et al. Telomeric DNA damage is irreparable and causes persistent DNA-damage-response activation. Nature Cell Biology 2012; 14(4): 355–365.
- Zeman MK, Cimprich KA. Causes and consequences of replication stress. Nat Cell Biol 2014; 16(1): 2–9.
- Di Micco R, Fumagalli M, Cicalese A et al. Oncogene-induced senescence is a DNA damage response triggered by DNA hyper-replication. Nature 2006; 444(7119): 638–642.
- Sarni D, Kerem B. Oncogene-induced replication stress drives genome instability and tumorigenesis. Int J Mol Sci 2017; 18(7): 1339.
- Béresová L, Veselá E, Chamrád I et al. Role of DNA repair factor xeroderma pigmentosum protein group C in response to replication stress as revealed by DNA fragile site affinity chromatography and quantitative proteomics. J Proteome Res 2016; 15(12): 4505–4517.
- Demaria M, O'Leary MN, Chang J et al. Cellular senescence promotes adverse effects of chemotherapy and cancer relapse. Cancer Discov 2017; 7(2): 165–176.
- Hudson MM, Ness KK, Gurney JG et al. Clinical ascertainment of health outcomes among adults treated for childhood cancer. JAMA 2013; 309(22): 2371–2381.
- Cupit-Link MC, Kirkland JL, Ness KK et al. Biology of premature ageing in survivors of cancer. ESMO Open 2017; 2(5): e000250.
- Navarro CL, Cau P, Lévy N. Molecular bases of progeroid syndromes. Hum Mol Genet 2006; 15(2): R151–R161.
- Shamanna RA, Croteau DL, Lee JH et al. Recent advances in understanding Werner syndrome. F1000Res 2017; 6: 1779.
- Vidak S, Foisner R. Molecular insights into the premature aging disease progeria. Histochem Cell Biol 2016; 145(4): 401–417.
- Wheaton K, Campuzano D, Ma W et al. Progerin-induced replication stress facilitates premature senescence in Hutchinson-Gilford progeria syndrome. Mol Cell Biol 2017; 37(14): e00659-16.
- Cordisco S, Tinaburri L, Teson M et al. Cockayne syndrome type A protein protects primary human keratinocytes from senescence. J Investig Dermatol 2019; 139(1): 38–50.
- de Renty C, Ellis NA. Bloom’s syndrome: why not premature aging? A comparison of the BLM and WRN helicases. Aging Res Rev 2016; 33: 36–51.
- Frontini M, Proietti-De-Santis L. Interaction between the Cockayne syndrome B and p53 proteins: implications for aging. Aging 2012; 4(2): 89–97.
- Zhan H, Suzuki T, Aizawa K et al. Ataxia telangiectasia mutated (ATM)-mediated DNA damage response in oxidative stress-induced vascular endothelial cell senescence. J Biol Chem 2010; 285(38): 29662–29670.
- Baker DJ, Wijshake T, Tchkonia T et al. Clearance of p16Ink4a-positive senescent cells delays ageing-associated disorders. Nature 2011; 479(7372): 232–236.
- Baker DJ, Childs BG, Durik M et al. Naturally occurring p16(Ink4a)-positive cells shorten healthy lifespan. Nature 2016; 530(7589): 184–189.
- Cruickshanks HA, McBryan T, Nelson DM et al. Senescent cells harbour features of the cancer epigenome. Nat Cell Biol 2013; 15(12): 1495–1506.
- Hickson LJ, Langhi Prata LGP, Bobart SA et al. Senolytics decrease senescent cells in humans: preliminary report from a clinical trial of dasatinib plus quercetin in individuals with diabetic kidney disease. EBioMedicine 2019; 47: 446–456.
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Addictology Allergology and clinical immunology Angiology Audiology Clinical biochemistry Dermatology & STDs Paediatric gastroenterology Paediatric surgery Paediatric cardiology Paediatric neurology Paediatric ENT Paediatric psychiatry Paediatric rheumatology Diabetology Pharmacy Vascular surgery Pain management Dental HygienistArticle was published in
Journal of Czech Physicians
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