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Advances in Experimental Medicine and BiologyVolume 1002, 2017, Pages 153-188

Mitotic dysfunction associated with aging hallmarks(Book Chapter)

  • aAging and Aneuploidy Laboratory, Instituto de Biologia Molecular e Celular, Instituto de Investigação e Inovação em Saúde – i3S, Universidade do Porto, Rua Alfredo Allen 208, Porto, 4200-135, Portugal
  • bCell Division Unit, Department of Experimental Biology, Faculdade de Medicina, Universidade do Porto, Alameda Prof. Hernâni Monteiro, Porto, 4200-319, Portugal

Abstract

Aging is a biological process characterized by the progressive deterioration of physiological functions known to be the main risk factor for chronic diseases and declining health. There has been an emerging connection between aging and aneuploidy, an aberrant number of chromosomes, even though the molecular mechanisms behind age-associated aneuploidy remain largely unknown. In recent years, several genetic pathways and biochemical processes controlling the rate of aging have been identified and proposed as aging hallmarks. Primary hallmarks that cause the accumulation of cellular damage include genomic instability, telomere attrition, epigenetic alterations and loss of proteostasis (López-Otín et al., Cell 153:1194–1217, 2013). Here we review the provocative link between these aging hallmarks and the loss of chromosome segregation fidelity during cell division, which could support the correlation between aging and aneuploidy seen over the past decades. Secondly, we review the systemic impacts of aneuploidy in cell physiology and emphasize how these include some of the primary hallmarks of aging. Based on the evidence, we propose a mutual causality between aging and aneuploidy, and suggest modulation of mitotic fidelity as a potential means to ameliorate healthy lifespan. © 2017, Springer International Publishing AG.

Author keywords

AgingAneuploidyEpigeneticsGenomic instabilityMitosisProteostasisTelomeres

Indexed keywords

EMTREE drug terms:chaperoneheat shock protein
EMTREE medical terms:agingAlzheimer diseaseaneuploidychaperone-mediated autophagychromatin assembly and disassemblychromosomal instabilitychromosome segregationDNA damageDNA methylationDown syndromegenomic instabilityhistone modificationhumanlaminopathymitosisnonhumannuclear laminapremature agingpriority journalprogeriaprotein homeostasisprotein misfoldingtelomere shorteningubiquitin proteasome systemubiquitinationageaginganimalcell aginggenetic epigenesisgeneticsgenotypemetabolismpathologyphenotype
MeSH:Age FactorsAgingAneuploidyAnimalsCell AgingChromosome SegregationEpigenesis, GeneticGenomic InstabilityGenotypeHumansMitosisPhenotypeTelomere Shortening
  • ISSN: 00652598
  • CODEN: AEMBA
  • Source Type: Book series
  • Original language: English
  • DOI: 10.1007/978-3-319-57127-0_7
  • PubMed ID: 28600786
  • Document Type: Book Chapter
  • Publisher: Springer New York LLC

  Logarinho, E.; Aging and Aneuploidy Laboratory, Instituto de Biologia Molecular e Celular, Instituto de Investigação e Inovação em Saúde – i3S, Universidade do Porto, Rua Alfredo Allen 208, Porto, Portugal;
© Copyright 2017 Elsevier B.V., All rights reserved.

Cited by 8 documents

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