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020 _a9783031550225
_9978-3-031-55022-5
024 7 _a10.1007/978-3-031-55022-5
_2doi
050 4 _aQH506
072 7 _aPSD
_2bicssc
072 7 _aSCI049000
_2bisacsh
072 7 _aPSD
_2thema
245 1 0 _aCellular and Molecular Aspects of Ageing
_h[electronic resource] /
_cedited by Valquiria Bueno.
250 _a1st ed. 2024.
264 1 _aCham :
_bSpringer Nature Switzerland :
_bImprint: Springer,
_c2024.
300 _aV, 158 p. 9 illus., 8 illus. in color.
_bonline resource.
336 _atext
_btxt
_2rdacontent
337 _acomputer
_bc
_2rdamedia
338 _aonline resource
_bcr
_2rdacarrier
347 _atext file
_bPDF
_2rda
505 0 _a1. Introduction: Daniela Frasca & Valquiria Bueno -- 2. Cellular Senescence: Laura Haynes -- 3. Genomic instability: Carlos López-Otín -- 4. Telomeres:Rodrigo do Tocantins C.S.Rodrigues -- 5. Epigenetic: Miriam Galvonas Jasiulionis -- 6. Proteostasis: Ana Maria Cuervo -- 7. Deregulated nutrient-sensing: Pedro Manoel M.M.Vieira -- 8. Mitochondria/Oxidative Stress: Tiago Rodrigues -- 9. Stem cell exhaustion: Michael D Milsom -- 10. Cell-to-cell communication: Ana O'Loghlen -- 11. Senescence-associated secretory phenotype (SASP): Janet M Lord.
520 _aEven though life expectancy increased in the last decades, ageing has been considered a strong risk factor for age-related diseases, disability and death. The further understanding of cellular and molecular aspects of ageing could predict the onset of diseases in advance, prevent functional decline and identify targets for interventions focused in healthy ageing. The hypothesis that organismal ageing and dysfunction is influenced by the accumulation of senescent cells had origin in Hayflick and Moorhead results from cultured human fibroblasts. It was shown that fibroblasts presented a limited capacity for proliferation reaching thus the state of irreversible growth arrest (replicative senescence). In 2011, van Deusen et al. showed that p16Ink4a accumulation was associated with premature ageing in a mouse model and the inactivation of the p16Ink4a gene mitigated the ageing phenotype. Thus, the cell cycle arrest due to the expression of p16Ink4a and p21CIP (cell cycle inhibitors) is the main characteristic of senescence. In addition to cellular senescence, the hallmarks of ageing include genomic instability, telomere shortening , epigenetic alterations, loss of proteostasis, deregulated nutrient-sensing, mitochondrial dysfunction, stem cell exhaustion, altered intercellular communication, and a pro-inflammatory senescence-associated secretory phenotype (SASP). In this book, researchers will comprehensively discuss relevant changes occurring at cellular and molecular levels (human and animal models) based on the hallmarks of ageing. The impact of lifestyle and benefits of physical activity and nutrition will be also discussed. Unravelling cellular and molecular aspects of ageing is crucial for the unanswered questions about ageing and for guiding interventions such as changes in lifestyle, senolytic (kills senescent cells), and senomorphic (interrupts deleterious intercellular communication) therapies.
650 0 _aMolecular biology.
650 0 _aCytology.
_967436
650 0 _aGenetics.
_968863
650 0 _aImmunology.
_969214
650 0 _aMedical sciences.
_965984
650 1 4 _aMolecular Biology.
650 2 4 _aCell Biology.
_967440
650 2 4 _aGenetics and Genomics.
_968866
650 2 4 _aImmunology.
_969214
650 2 4 _aHealth Sciences.
_965987
700 1 _aBueno, Valquiria.
_eeditor.
_4edt
_4http://id.loc.gov/vocabulary/relators/edt
_974059
710 2 _aSpringerLink (Online service)
773 0 _tSpringer Nature eBook
776 0 8 _iPrinted edition:
_z9783031550218
776 0 8 _iPrinted edition:
_z9783031550232
776 0 8 _iPrinted edition:
_z9783031550249
856 4 0 _uhttps://doi.org/10.1007/978-3-031-55022-5
912 _aZDB-2-SBL
912 _aZDB-2-SXB
999 _c58682
_d58682