dc.contributor.author | Krupa, Renata | |
dc.contributor.author | Sławińska, Natalia | |
dc.date.accessioned | 2021-12-13T12:05:24Z | |
dc.date.available | 2021-12-13T12:05:24Z | |
dc.date.issued | 2020 | |
dc.identifier.citation | Sławińska, N.; Krupa, R. Molecular Aspects of Senescence and Organismal Ageing—DNA Damage Response, Telomeres, Inflammation and Chromatin. Int. J. Mol. Sci. 2021, 22, 590. https://doi.org/10.3390/ ijms22020590 | pl_PL |
dc.identifier.issn | 1661-6596 | |
dc.identifier.uri | http://hdl.handle.net/11089/39988 | |
dc.description.abstract | Cells can become senescent in response to stress. Senescence is a process characterised by a stable proliferative arrest. Sometimes it can be beneficial—for example, it can suppress tumour development or take part in tissue repair. On the other hand, studies show that it is also involved in the ageing process. DNA damage response (DDR) is triggered by DNA damage or telomere shortening during cell division. When left unresolved, it may lead to the activation of senescence. Senescent cells secrete certain proteins in larger quantities. This phenomenon is referred to as senescence-associated secretory phenotype (SASP). SASP can induce senescence in other cells; evidence suggests that overabundance of senescent cells contributes to ageing. SASP proteins include proinflammatory cytokines and metalloproteinases, which degrade the extracellular matrix. Shortening of telomeres is another feature associated with organismal ageing. Older organisms have shorter telomeres. Restoring telomerase activity in mice not only slowed but also partially reversed the symptoms of ageing. Changes in chromatin structure during senescence include heterochromatin formation or decondensation and loss of H1 histones. During organismal ageing, cells can experience heterochromatin loss, DNA demethylation and global histone loss. Cellular and organismal ageing are both complex processes with many aspects that are often related. The purpose of this review is to bring some of these aspects forward and provide details regarding them. | pl_PL |
dc.language.iso | en | pl_PL |
dc.publisher | MDPI | pl_PL |
dc.relation.ispartofseries | International Journal of Molecular Sciences;2 | |
dc.rights | Uznanie autorstwa 4.0 Międzynarodowe | * |
dc.rights.uri | http://creativecommons.org/licenses/by/4.0/ | * |
dc.subject | ageing | pl_PL |
dc.subject | senescence | pl_PL |
dc.subject | DNA damage response | pl_PL |
dc.subject | telomeres | pl_PL |
dc.subject | inflammation | pl_PL |
dc.subject | chromatin | pl_PL |
dc.subject | SASP | pl_PL |
dc.title | Molecular Aspects of Senescence and Organismal Ageing—DNA Damage Response, Telomeres, Inflammation and Chromatin | pl_PL |
dc.type | Article | pl_PL |
dc.page.number | 16 | pl_PL |
dc.contributor.authorAffiliation | Laboratory of Medical Genetics, Faculty of Biology and Environmental Protection, University of Lodz, 90-236 Lodz, Poland | pl_PL |
dc.contributor.authorAffiliation | Laboratory of Medical Genetics, Faculty of Biology and Environmental Protection, University of Lodz, 90-236 Lodz, Poland | pl_PL |
dc.identifier.eissn | 1422-0067 | |
dc.references | Jeyapalan, J.C.; Ferreira, M.; Sedivy, J.M.; Herbig, U. Accumulation of senescent cells in mitotic tissue of aging primates. Mech. Age. Dev. 2007, 128, 36–44. | pl_PL |
dc.references | Salama, R.; Sadaie, M.; Hoare, M.; Narita, M. Cellular senescence and its effector programs. Genes Dev. 2014, 28, 99–114. | pl_PL |
dc.references | Van Deursen, J.M. The role of senescent cells in ageing. Nature 2014, 509, 439–446. | pl_PL |
dc.references | Polo, S.E.; Jackson, S.P. Dynamics of DNA damage response proteins at DNA breaks: A focus on protein modifications. Genes Dev. 2011, 25, 409–433. | pl_PL |
dc.references | Rossiello, F.; Herbig, U.; Longhese, M.P.; Fumagalli, M.; d’Adda di Fagagna, F. Irreparable telomeric DNA damage and persistent DDR signalling as a shared causative mechanism of cellular senescence and ageing. Curr. Opin. Genet. Dev. 2014, 26, 89–95. | pl_PL |
dc.references | White, R.R.; Milholland, B.; de Bruin, A.; Curran, S.; Laberge, R.M.; van Steeg, H.; Campisi, J.; Maslov, A.Y.; Vijg, J. Controlled induction of DNA double-strand breaks in the mouse liver induces features of tissue ageing. Nat. Commun. 2015, 6, 6790. | pl_PL |
dc.references | Mehta, A.; Haber, J.E. Sources of DNA double-strand breaks and models of recombinational DNA repair. Cold Spring Harb. Perspect. Biol. 2014, 6, a016428. | pl_PL |
dc.references | Watts, F.Z. Repair of DNA Double-Strand Breaks in Heterochromatin. Biomolecules 2016, 6, 47. | pl_PL |
dc.references | Chiruvella, K.K.; Liang, Z.; Wilson, T.E. Repair of double-strand breaks by end joining. Cold Spring Harb. Perspect. Biol. 2013, 5, a012757. | pl_PL |
dc.references | Doksani, Y. The Response to DNA Damage at Telomeric Repeats and Its Consequences for Telomere Function. Genes 2019, 10, 318. | pl_PL |
dc.references | Mateos-Gomez, P.A.; Gong, F.; Nair, N.; Miller, K.M.; Lazzerini-Denchi, E.; Sfeir, A. Mammalian polymerase theta promotes alternative NHEJ and suppresses recombination. Nature 2015, 518, 254–257. | pl_PL |
dc.references | 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. Aging Cell 2009, 8, 311–323. | pl_PL |
dc.references | Rodier, F.; Munoz, D.P.; Teachenor, R.; Chu, V.; Le, O.; Bhaumik, D.; Coppe, J.P.; Campeau, E.; Beausejour, C.M.; Kim, S.H.; et al. DNA-SCARS: Distinct nuclear structures that sustain damage-induced senescence growth arrest and inflammatory cytokine secretion. J. Cell Sci. 2011, 124, 68–81. | pl_PL |
dc.references | Fumagalli, M.; Rossiello, F.; Mondello, C.; d’Adda di Fagagna, F. Stable cellular senescence is associated with persistent DDR activation. PLoS ONE 2014, 9, e110969. | pl_PL |
dc.references | Blackburn, E.H. Telomeres. Trends Biochem. Sci. 1991, 16, 378–381. | pl_PL |
dc.references | Blackburn, E.H. Structure and function of telomeres. Nature 1991, 350, 569–573. | pl_PL |
dc.references | Meyne, J.; Ratliff, R.L.; Moyzis, R.K. Conservation of the human telomere sequence (TTAGGG)n among vertebrates. Proc. Natl. Acad. Sci. USA 1989, 86, 7049–7053. | pl_PL |
dc.references | Moyzis, R.K.; Buckingham, J.M.; Cram, L.S.; Dani, M.; Deaven, L.L.; Jones, M.D.; Meyne, J.; Ratliff, R.L.; Wu, J.R. A highly conserved repetitive DNA sequence, (TTAGGG)n, present at the telomeres of human chromosomes. Proc. Natl. Acad. Sci. USA 1988, 85, 6622–6626. | pl_PL |
dc.references | Makarov, V.L.; Hirose, Y.; Langmore, J.P. Long G tails at both ends of human chromosomes suggest a C strand degradation mechanism for telomere shortening. Cell 1997, 88, 657–666. | pl_PL |
dc.references | Griffith, J.D.; Comeau, L.; Rosenfield, S.; Stansel, R.M.; Bianchi, A.; Moss, H.; de Lange, T. Mammalian telomeres end in a large duplex loop. Cell 1999, 97, 503–514. | pl_PL |
dc.references | Benarroch-Popivker, D.; Pisano, S.; Mendez-Bermudez, A.; Lototska, L.; Kaur, P.; Bauwens, S.; Djerbi, N.; Latrick, C.M.; Fraisier, V.; Pei, B.; et al. TRF2-mediated control of telomere DNA topology as a mechanism for chromosome-end protection. Mol. Cell 2016, 61, 274–286. | pl_PL |
dc.references | De Lange, T. Shelterin: The protein complex that shapes and safeguards human telomeres. Genes Dev. 2005, 19, 2100–2110. | pl_PL |
dc.references | De Lange, T. Shelterin-mediated telomere protection. Annu. Rev. Genet. 2018, 52, 223–247. | pl_PL |
dc.references | Broccoli, D.; Smogorzewska, A.; Chong, L.; de Lange, T. Human telomeres contain two distinct Myb-related proteins, TRF1 and TRF2. Nat. Genet. 1997, 17, 231–235. | pl_PL |
dc.references | Hu, C.; Rai, R.; Huang, C.; Broton, C.; Long, J.; Xu, Y.; Xue, J.; Lei, M.; Chang, S.; Chen, Y. Structural and functional analyses of the mammalian TIN2-TPP1-TRF2 telomeric complex. Cell Res. 2017, 27, 1485–1502. | pl_PL |
dc.references | Lei, M.; Podell, E.R.; Cech, T.R. Structure of human POT1 bound to telomeric single-stranded DNA provides a model for chromosome end-protection. Nat. Struct. Mol. Biol. 2004, 11, 1223–1229. | pl_PL |
dc.references | Veverka, P.; Janovic, T.; Hofr, C. Quantitative biology of human shelterin and telomerase: Searching for the weakest point. Int. J. Mol. Sci. 2019, 20, 3186. | pl_PL |
dc.references | Fumagalli, M.; Rossiello, F.; Clerici, M.; Barozzi, S.; Cittaro, D.; Kaplunov, J.M.; Bucci, G.; Dobreva, M.; Matti, V.; Beausejour, C.M.; et al. Telomeric DNA damage is irreparable and causes persistent DNA-damage-response activation. Nat. Cell Biol. 2012, 14, 355–365. | pl_PL |
dc.references | Smogorzewska, A.; de Lange, T. Different telomere damage signaling pathways in human and mouse cells. EMBO J. 2002, 21, 4338–4348. | pl_PL |
dc.references | Gomes, N.M.; Ryder, O.A.; Houck, M.L.; Charter, S.J.; Walker, W.; Forsyth, N.R.; Austad, S.N.; Venditti, C.; Pagel, M.; Shay, J.W.; et al. Comparative biology of mammalian telomeres: Hypotheses on ancestral states and the roles of telomeres in longevity determination. Aging Cell 2011, 10, 761–768. | pl_PL |
dc.references | Gardner, J.P.; Kimura, M.; Chai, W.; Durrani, J.F.; Tchakmakjian, L.; Cao, X.; Lu, X.; Li, G.; Peppas, A.P.; Skurnick, J.; et al. Telomere dynamics in macaques and humans. J. Gerontol. A Biol. Sci. Med. Sci. 2007, 62, 367–374. | pl_PL |
dc.references | Lansdorp, P.M.; Verwoerd, N.P.; van de Rijke, F.M.; Dragowska, V.; Little, M.T.; Dirks, R.W.; Raap, A.K.; Tanke, H.J. Heterogeneity in telomere length of human chromosomes. Hum. Mol. Genet. 1996, 5, 685–691. | pl_PL |
dc.references | Haussmann, M.F.; Winkler, D.W.; O’Reilly, K.M.; Huntington, C.E.; Nisbet, I.C.; Vleck, C.M. Telomeres shorten more slowly in long-lived birds and mammals than in short-lived ones. Proc. Biol. Sci. 2003, 270, 1387–1392. | pl_PL |
dc.references | Karlseder, J.; Smogorzewska, A.; de Lange, T. Senescence induced by altered telomere state, not telomere loss. Science 2002, 295, 2446–2449. | pl_PL |
dc.references | Palm, W.; de Lange, T. How shelterin protects mammalian telomeres. Annu. Rev. Genet. 2008, 42, 301–334. | pl_PL |
dc.references | Bar, C.; Blasco, M.A. Telomeres and telomerase as therapeutic targets to prevent and treat age-related diseases. F1000Research 2016, 5. | pl_PL |
dc.references | Hewitt, G.; Jurk, D.; Marques, F.D.; Correia-Melo, C.; Hardy, T.; Gackowska, A.; Anderson, R.; Taschuk, M.; Mann, J.; Passos, J.F. Telomeres are favoured targets of a persistent DNA damage response in ageing and stress-induced senescence. Nat. Commun. 2012, 3, 708. | pl_PL |
dc.references | D’Adda di Fagagna, F.; Reaper, P.M.; Clay-Farrace, L.; Fiegler, H.; Carr, P.; Von Zglinicki, T.; Saretzki, G.; Carter, N.P.; Jackson, S.P. A DNA damage checkpoint response in telomere-initiated senescence. Nature 2003, 426, 194–198. | pl_PL |
dc.references | Takai, H.; Smogorzewska, A.; de Lange, T. DNA damage foci at dysfunctional telomeres. Curr. Biol. 2003, 13, 1549–1556. | pl_PL |
dc.references | Herbig, U.; Jobling, W.A.; Chen, B.P.; Chen, D.J.; Sedivy, J.M. Telomere shortening triggers senescence of human cells through a pathway involving ATM, p53, and p21(CIP1), but not p16(INK4a). Mol. Cell 2004, 14, 501–513. | pl_PL |
dc.references | Coppe, J.P.; Patil, C.K.; Rodier, F.; Sun, Y.; Munoz, D.P.; Goldstein, J.; Nelson, P.S.; Desprez, P.Y.; Campisi, J. Senescence-associated secretory phenotypes reveal cell-nonautonomous functions of oncogenic RAS and the p53 tumor suppressor. PLoS Biol. 2008, 6, 2853–2868. | pl_PL |
dc.references | Shelton, D.N.; Chang, E.; Whittier, P.S.; Choi, D.; Funk, W.D. Microarray analysis of replicative senescence. Curr. Biol. 1999, 9, 939–945. | pl_PL |
dc.references | Childs, B.G.; Durik, M.; Baker, D.J.; van Deursen, J.M. Cellular senescence in aging and age-related disease: From mechanisms to therapy. Nat. Med. 2015, 21, 1424–1435. | pl_PL |
dc.references | Kuilman, T.; Michaloglou, C.; Vredeveld, L.C.; Douma, S.; van Doorn, R.; Desmet, C.J.; Aarden, L.A.; Mooi, W.J.; Peeper, D.S. Oncogene-induced senescence relayed by an interleukin-dependent inflammatory network. Cell 2008, 133, 1019–1031. | pl_PL |
dc.references | Krtolica, A.; Parrinello, S.; Lockett, S.; Desprez, P.Y.; Campisi, J. Senescent fibroblasts promote epithelial cell growth and tumorigenesis: A link between cancer and aging. Proc. Natl. Acad. Sci. USA 2001, 98, 12072–12077. | pl_PL |
dc.references | Ma, Y.; Ren, Y.; Dai, Z.J.; Wu, C.J.; Ji, Y.H.; Xu, J. IL-6, IL-8 and TNF-alpha levels correlate with disease stage in breast cancer patients. Adv. Clin. Exp. Med. 2017, 26, 421–426. | pl_PL |
dc.references | Rodier, F.; Coppe, J.P.; Patil, C.K.; Hoeijmakers, W.A.; Munoz, D.P.; Raza, S.R.; Freund, A.; Campeau, E.; Davalos, A.R.; Campisi, J. Persistent DNA damage signalling triggers senescence-associated inflammatory cytokine secretion. Nat. Cell Biol. 2009, 11, 973–979. | pl_PL |
dc.references | Hayakawa, T.; Iwai, M.; Aoki, S.; Takimoto, K.; Maruyama, M.; Maruyama, W.; Motoyama, N. SIRT1 suppresses the senescenceassociated secretory phenotype through epigenetic gene regulation. PLoS ONE 2015, 10, e0116480. | pl_PL |
dc.references | Oberdoerffer, P.; Michan, S.; McVay, M.; Mostoslavsky, R.; Vann, J.; Park, S.K.; Hartlerode, A.; Stegmuller, J.; Hafner, A.; Loerch, P.; et al. SIRT1 redistribution on chromatin promotes genomic stability but alters gene expression during aging. Cell 2008, 135, 907–918. | pl_PL |
dc.references | Hwang, J.W.; Yao, H.; Caito, S.; Sundar, I.K.; Rahman, I. Redox regulation of SIRT1 in inflammation and cellular senescence. Free Radic. Biol. Med. 2013, 61, 95–110. | pl_PL |
dc.references | Narita, M.; Nunez, S.; Heard, E.; Narita, M.; Lin, A.W.; Hearn, S.A.; Spector, D.L.; Hannon, G.J.; Lowe, S.W. Rb-mediated heterochromatin formation and silencing of E2F target genes during cellular senescence. Cell 2003, 113, 703–716. | pl_PL |
dc.references | Funayama, R.; Saito, M.; Tanobe, H.; Ishikawa, F. Loss of linker histone H1 in cellular senescence. J. Cell Biol. 2006, 175, 869–880. | pl_PL |
dc.references | Zhang, R.; Chen, W.; Adams, P.D. Molecular dissection of formation of senescence-associated heterochromatin foci. Mol. Cell Biol. 2007, 27, 2343–2358 | pl_PL |
dc.references | Zhang, R.; Poustovoitov, M.V.; Ye, X.; Santos, H.A.; Chen, W.; Daganzo, S.M.; Erzberger, J.P.; Serebriiskii, I.G.; Canutescu, A.A.; Dunbrack, R.L.; et al. Formation of MacroH2A-containing senescence-associated heterochromatin foci and senescence driven by ASF1a and HIRA. Dev. Cell 2005, 8, 19–30. | pl_PL |
dc.references | Freund, A.; Laberge, R.M.; Demaria, M.; Campisi, J. Lamin B1 loss is a senescence-associated biomarker. Mol. Biol. Cell 2012, 23, 2066–2075. | pl_PL |
dc.references | Shah, P.P.; Donahue, G.; Otte, G.L.; Capell, B.C.; Nelson, D.M.; Cao, K.; Aggarwala, V.; Cruickshanks, H.A.; Rai, T.S.; McBryan, T.; et al. Lamin B1 depletion in senescent cells triggers large-scale changes in gene expression and the chromatin landscape. Genes Dev. 2013, 27, 1787–1799. | pl_PL |
dc.references | Shimi, T.; Pfleghaar, K.; Kojima, S.; Pack, C.G.; Solovei, I.; Goldman, A.E.; Adam, S.A.; Shumaker, D.K.; Kinjo, M.; Cremer, T.; et al. The A- and B-type nuclear lamin networks: Microdomains involved in chromatin organization and transcription. Genes Dev. 2008, 22, 3409–3421. | pl_PL |
dc.references | Shimi, T.; Butin-Israeli, V.; Adam, S.A.; Hamanaka, R.B.; Goldman, A.E.; Lucas, C.A.; Shumaker, D.K.; Kosak, S.T.; Chandel, N.S.; Goldman, R.D. The role of nuclear lamin B1 in cell proliferation and senescence. Genes Dev. 2011, 25, 2579–2593. | pl_PL |
dc.references | Swanson, E.C.; Manning, B.; Zhang, H.; Lawrence, J.B. Higher-order unfolding of satellite heterochromatin is a consistent and early event in cell senescence. J. Cell Biol. 2013, 203, 929–942. | pl_PL |
dc.references | Honig, L.S.; Kang, M.S.; Schupf, N.; Lee, J.H.; Mayeux, R. Association of shorter leukocyte telomere repeat length with dementia and mortality. Arch. Neurol. 2012, 69, 1332–1339. | pl_PL |
dc.references | Vera, E.; Bernardes de Jesus, B.; Foronda, M.; Flores, J.M.; Blasco, M.A. Telomerase reverse transcriptase synergizes with calorie restriction to increase health span and extend mouse longevity. PLoS ONE 2013, 8, e53760. | pl_PL |
dc.references | Brown, T.A. Genomes, 2nd ed.; Wiley-Liss: Oxford, UK, 2002. | pl_PL |
dc.references | Carneiro, M.C.; Henriques, C.M.; Nabais, J.; Ferreira, T.; Carvalho, T.; Ferreira, M.G. Short telomeres in key tissues initiate local and systemic aging in Zebrafish. PLoS Genet. 2016, 12, e1005798. | pl_PL |
dc.references | Du, X.; Shen, J.; Kugan, N.; Furth, E.E.; Lombard, D.B.; Cheung, C.; Pak, S.; Luo, G.; Pignolo, R.J.; DePinho, R.A.; et al. Telomere shortening exposes functions for the mouse Werner and Bloom syndrome genes. Mol. Cell Biol. 2004, 24, 8437–8446. | pl_PL |
dc.references | Bertuch, A.A. The molecular genetics of the telomere biology disorders. RNA Biol. 2016, 13, 696–706. | pl_PL |
dc.references | Grill, S.; Nandakumar, J. Molecular mechanisms of telomere biology disorders. J. Biol. Chem. 2020. | pl_PL |
dc.references | Dokal, I. Dyskeratosis congenita. Hematol. Am. Soc. Hematol. Educ. Prog. 2011, 2011, 480–486. | pl_PL |
dc.references | Armanios, M.; Blackburn, E.H. The telomere syndromes. Nat. Rev. Genet. 2012, 13, 693–704. | pl_PL |
dc.references | Niewisch, M.R.; Savage, S.A. An update on the biology and management of dyskeratosis congenita and related telomere biology disorders. Exp. Rev. Hematol. 2019, 12, 1037–1052. | pl_PL |
dc.references | Birch, J.; Anderson, R.K.; Correia-Melo, C.; Jurk, D.; Hewitt, G.; Marques, F.M.; Green, N.J.; Moisey, E.; Birrell, M.A.; Belvisi, M.G.; et al. DNA damage response at telomeres contributes to lung aging and chronic obstructive pulmonary disease. Am. J. Physiol. Lung Cell Mol. Physiol. 2015, 309, L1124–L1137. | pl_PL |
dc.references | Jaskelioff, M.; Muller, F.L.; Paik, J.H.; Thomas, E.; Jiang, S.; Adams, A.C.; Sahin, E.; Kost-Alimova, M.; Protopopov, A.; Cadinanos, J.; et al. Telomerase reactivation reverses tissue degeneration in aged telomerase-deficient mice. Nature 2011, 469, 102–106. | pl_PL |
dc.references | Ge, J.; Li, C.; Li, C.; Huang, Z.; Zeng, J.; Han, L.; Wang, Q. SIRT6 participates in the quality control of aged oocytes via modulating telomere function. Aging 2019, 11, 1965–1976. | pl_PL |
dc.references | Nelson, G.; Wordsworth, J.; Wang, C.; Jurk, D.; Lawless, C.; Martin-Ruiz, C.; von Zglinicki, T. A senescent cell bystander effect: Senescence-induced senescence. Aging Cell 2012, 11, 345–349. | pl_PL |
dc.references | Rea, I.M.; Gibson, D.S.; McGilligan, V.; McNerlan, S.E.; Alexander, H.D.; Ross, O.A. Age and Age-Related Diseases: Role of Inflammation Triggers and Cytokines. Front. Immunol. 2018, 9, 586. | pl_PL |
dc.references | Enkhmaa, B.; Anuurad, E.; Zhang, W.; Kim, K.; Berglund, L. Diverging trajectory patterns of systemic versus vascular inflammation over age in healthy Caucasians and African-Americans. Atherosclerosis 2015, 239, 509–515. | pl_PL |
dc.references | Freund, A.; Orjalo, A.V.; Desprez, P.Y.; Campisi, J. Inflammatory networks during cellular senescence: Causes and consequences. Trends Mol. Med. 2010, 16, 238–246. | pl_PL |
dc.references | Arai, Y.; Martin-Ruiz, C.M.; Takayama, M.; Abe, Y.; Takebayashi, T.; Koyasu, S.; Suematsu, M.; Hirose, N.; von Zglinicki, T. Inflammation, but not telomere length, predicts successful ageing at extreme old age: A longitudinal study of semi-supercentenarians. EBio Med. 2015, 2, 1549–1558. | pl_PL |
dc.references | Xu, M.; Tchkonia, T.; Ding, H.; Ogrodnik, M.; Lubbers, E.R.; Pirtskhalava, T.; White, T.A.; Johnson, K.O.; Stout, M.B.; Mezera, V.; et al. JAK inhibition alleviates the cellular senescence-associated secretory phenotype and frailty in old age. Proc. Natl. Acad. Sci. USA 2015, 112, E6301–E6310. | pl_PL |
dc.references | Xin, P.; Xu, X.; Deng, C.; Liu, S.; Wang, Y.; Zhou, X.; Ma, H.; Wei, D.; Sun, S. The role of JAK/STAT signaling pathway and its inhibitors in diseases. Int. Immunopharmacol. 2020, 80, 106210. | pl_PL |
dc.references | Stabile, H.; Scarno, G.; Fionda, C.; Gismondi, A.; Santoni, A.; Gadina, M.; Sciume, G. JAK/STAT signaling in regulation of innate lymphoid cells: The gods before the guardians. Immunol. Rev. 2018, 286, 148–159. | pl_PL |
dc.references | Owen, K.L.; Brockwell, N.K.; Parker, B.S. JAK-STAT signaling: A double-edged sword of immune regulation and cancer progression. Cancers 2019, 11, 2002. | pl_PL |
dc.references | Sorensen, C.E.; Tritsaris, K.; Reibel, J.; Lauritzen, M.; Mortensen, E.L.; Osler, M.; Pedersen, A.M. Elevated p16ink4a Expression in Human Labial Salivary Glands as a Potential Correlate of Cognitive Aging in Late Midlife. PLoS ONE 2016, 11, e0152612. | pl_PL |
dc.references | Hall, B.M.; Balan, V.; Gleiberman, A.S.; Strom, E.; Krasnov, P.; Virtuoso, L.P.; Rydkina, E.; Vujcic, S.; Balan, K.; Gitlin, I.; et al. Aging of mice is associated with p16(Ink4a)- and beta-galactosidase-positive macrophage accumulation that can be induced in young mice by senescent cells. Aging 2016, 8, 1294–1315. | pl_PL |
dc.references | Baar, M.P.; Brandt, R.M.C.; Putavet, D.A.; Klein, J.D.D.; Derks, K.W.J.; Bourgeois, B.R.M.; Stryeck, S.; Rijksen, Y.; van Willigenburg, H.; Feijtel, D.A.; et al. Targeted apoptosis of senescent cells restores tissue homeostasis in response to chemotoxicity and aging. Cell 2017, 169, 132–147 e116. | pl_PL |
dc.references | Greer, E.L.; Becker, B.; Latza, C.; Antebi, A.; Shi, Y. Mutation of C. elegans demethylase spr-5 extends transgenerational longevity. Cell Res. 2016, 26, 229–238. | pl_PL |
dc.references | Sidler, C.; Kovalchuk, O.; Kovalchuk, I. Epigenetic regulation of cellular senescence and aging. Front. Genet. 2017, 8, 138. | pl_PL |
dc.references | Larson, K.; Yan, S.J.; Tsurumi, A.; Liu, J.; Zhou, J.; Gaur, K.; Guo, D.; Eickbush, T.H.; Li, W.X. Heterochromatin formation promotes longevity and represses ribosomal RNA synthesis. PLoS Genet. 2012, 8, e1002473. | pl_PL |
dc.references | Jones, P.A. Functions of DNA methylation: Islands, start sites, gene bodies and beyond. Nat. Rev. Genet. 2012, 13, 484–492. | pl_PL |
dc.references | Ehrlich, M.; Wang, R.Y. 5-Methylcytosine in eukaryotic DNA. Science 1981, 212, 1350–1357. | pl_PL |
dc.references | Ehrlich, M.; Gama-Sosa, M.A.; Huang, L.H.; Midgett, R.M.; Kuo, K.C.; McCune, R.A.; Gehrke, C. Amount and distribution of 5-methylcytosine in human DNA from different types of tissues of cells. Nucl. Acids Res. 1982, 10, 2709–2721. | pl_PL |
dc.references | Doerfler, W. The significance of DNA methylation patterns: Promoter inhibition by sequence-specific methylation is one functional consequence. Philos. Trans. R. Soc. Lond. B Biol. Sci. 1990, 326, 253–265. | pl_PL |
dc.references | Saxonov, S.; Berg, P.; Brutlag, D.L. A genome-wide analysis of CpG dinucleotides in the human genome distinguishes two distinct classes of promoters. Proc. Natl. Acad. Sci. USA 2006, 103, 1412–1417. | pl_PL |
dc.references | Gopalan, S.; Carja, O.; Fagny, M.; Patin, E.; Myrick, J.W.; McEwen, L.M.; Mah, S.M.; Kobor, M.S.; Froment, A.; Feldman, M.W.; et al. Trends in DNA methylation with age replicate across diverse human populations. Genetics 2017, 206, 1659–1674. | pl_PL |
dc.references | Wilson, V.L.; Smith, R.A.; Ma, S.; Cutler, R.G. Genomic 5-methyldeoxycytidine decreases with age. J. Biol. Chem. 1987, 262, 9948–9951. | pl_PL |
dc.references | Choi, H.; Joe, S.; Nam, H. Development of tissue-specific age predictors using DNA methylation data. Genes 2019, 10, 888. | pl_PL |
dc.references | Jung, S.E.; Shin, K.J.; Lee, H.Y. DNA methylation-based age prediction from various tissues and body fluids. BMB Rep. 2017, 50, 546–553. | pl_PL |
dc.references | Cui, X.L.; Nie, J.; Ku, J.; Dougherty, U.; West-Szymanski, D.C.; Collin, F.; Ellison, C.K.; Sieh, L.; Ning, Y.; Deng, Z.; et al. A human tissue map of 5-hydroxymethylcytosines exhibits tissue specificity through gene and enhancer modulation. Nat. Commun. 2020, 11, 6161. | pl_PL |
dc.references | Cho, S.; Jung, S.E.; Hong, S.R.; Lee, E.H.; Lee, J.H.; Lee, S.D.; Lee, H.Y. Independent validation of DNA-based approaches for age prediction in blood. Forens. Sci. Int. Genet. 2017, 29, 250–256. | pl_PL |
dc.references | Hong, S.R.; Jung, S.E.; Lee, E.H.; Shin, K.J.; Yang, W.I.; Lee, H.Y. DNA methylation-based age prediction from saliva: High age predictability by combination of 7 CpG markers. Forens. Sci. Int. Genet. 2017, 29, 118–125. | pl_PL |
dc.references | Naue, J.; Hoefsloot, H.C.J.; Mook, O.R.F.; Rijlaarsdam-Hoekstra, L.; van der Zwalm, M.C.H.; Henneman, P.; Kloosterman, A.D.; Verschure, P.J. Chronological age prediction based on DNA methylation: Massive parallel sequencing and random forest regression. Forens. Sci. Int. Genet. 2017, 31, 19–28. | pl_PL |
dc.references | Eipel, M.; Mayer, F.; Arent, T.; Ferreira, M.R.; Birkhofer, C.; Gerstenmaier, U.; Costa, I.G.; Ritz-Timme, S.; Wagner, W. Epigenetic age predictions based on buccal swabs are more precise in combination with cell type-specific DNA methylation signatures. Aging 2016, 8, 1034–1048. | pl_PL |
dc.references | Tasselli, L.; Zheng, W.; Chua, K.F. SIRT6: Novel mechanisms and links to aging and disease. Trends Endocrinol. Metab. 2017, 28, 168–185. | pl_PL |
dc.contributor.authorEmail | renata.krupa@biol.uni.lodz.pl | pl_PL |
dc.contributor.authorEmail | natalia.slawinska@edu.uni.lodz.pl | pl_PL |
dc.identifier.doi | 10.3390/ijms22020590 | |
dc.relation.volume | 22 | pl_PL |
dc.discipline | nauki biologiczne | pl_PL |