04432nam a22005175i 4500 978-3-031-55022-5 DE-He213 20260730115144.0 cr nn 008mamaa 240326s2024 sz | s |||| 0|eng d 9783031550225 10.1007/978-3-031-55022-5 doi EG-CaUEC eng EG-CaUEC EG-CaUEC rda 572 23 C.E.L Cellular and Molecular Aspects of Ageing [electronic resource] / edited by Valquiria Bueno. 1st ed. 2024. Cham : Springer Nature Switzerland : Imprint: Springer, 2024. V, 158 p. 9 illus., 8 illus. in color. online resource. text txt rdacontent computer c rdamedia online resource cr rdacarrier text file PDF rda 1. 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. Even 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. Molecular biology. Cytology. 94 Genetics. Immunology. Medical sciences. 557 Molecular Biology. Cell Biology. 100 Genetics and Genomics. 98 Immunology. Health Sciences. 558 Bueno, Valquiria. editor. edt http://id.loc.gov/vocabulary/relators/edt 559 SpringerLink (Online service) 9 Springer Nature eBook Printed edition: 9783031550218 Printed edition: 9783031550232 Printed edition: 9783031550249 https://library.uec.edu.eg/cgi-bin/koha/opac-retrieve-file.pl?id=a6ba090852a7853f9c549a0914bb3ad3 ddc EBK 0 Electronic resource ASIS ONLINE ONLINE ONLINE Springer Nature 2016-2024 imprints in 17 collections 20240417 Y Y ONLINE 146 146