Genomic instability and aging
Research output: Chapter in Book/Report/Conference proceeding › Book chapter › Research › peer-review
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Genomic instability and aging. / Li, Zhiquan; Anugula, Sharath; Rasmussen, Lene Juel.
Aging: From Fundamental Biology to Societal Impact. ed. / Paulo J. Oliveira; João O. Malva. Academic Press, 2022. p. 275-295.Research output: Chapter in Book/Report/Conference proceeding › Book chapter › Research › peer-review
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TY - CHAP
T1 - Genomic instability and aging
AU - Li, Zhiquan
AU - Anugula, Sharath
AU - Rasmussen, Lene Juel
N1 - Publisher Copyright: © 2023 Elsevier Inc. All rights reserved.
PY - 2022
Y1 - 2022
N2 - Aging is a complex process of damage accumulation causing a functional decline. Several hallmarks of aging have been identified, of which, genomic instability plays a critical role in aging and age-related diseases and closely interacts with other hallmarks of aging. The genome is constantly challenged by exogenous DNA damaging sources, such as ionizing radiation, ultraviolet, and chemicals. But also, endogenous DNA damage caused by alkylation and hydrolysis can lead to chromosomal aberrations, mutations, and epimutations, eventually causing genomic instability and cellular dysfunction. The stressor-induced alterations include chromosomal (chromosome aneuploidy, chromosomal rearrangements, and fragile sites), genomic (increased genetic variability and mutated nucleic acid sequences), replicative (replication stress), and transcriptional impairments. In response to these damages, a wide range of sophisticated repair mechanisms have evolved to repair different types of damage to preserve genomic integrity, such as proper chromosome segregation, efficient DNA damage repair, and faithful DNA replication, to maintain normal function and promote organismal survival. Mammalian DNA damage response systems mainly comprise nonhomologous end joining, homologous recombination, nucleotide excision repair, base excision repair, mismatch repair, direct reversal repair, and translesion DNA synthesis. To ensure genomic stability there is crosstalk and redundancy between the different DNA repair pathways.
AB - Aging is a complex process of damage accumulation causing a functional decline. Several hallmarks of aging have been identified, of which, genomic instability plays a critical role in aging and age-related diseases and closely interacts with other hallmarks of aging. The genome is constantly challenged by exogenous DNA damaging sources, such as ionizing radiation, ultraviolet, and chemicals. But also, endogenous DNA damage caused by alkylation and hydrolysis can lead to chromosomal aberrations, mutations, and epimutations, eventually causing genomic instability and cellular dysfunction. The stressor-induced alterations include chromosomal (chromosome aneuploidy, chromosomal rearrangements, and fragile sites), genomic (increased genetic variability and mutated nucleic acid sequences), replicative (replication stress), and transcriptional impairments. In response to these damages, a wide range of sophisticated repair mechanisms have evolved to repair different types of damage to preserve genomic integrity, such as proper chromosome segregation, efficient DNA damage repair, and faithful DNA replication, to maintain normal function and promote organismal survival. Mammalian DNA damage response systems mainly comprise nonhomologous end joining, homologous recombination, nucleotide excision repair, base excision repair, mismatch repair, direct reversal repair, and translesion DNA synthesis. To ensure genomic stability there is crosstalk and redundancy between the different DNA repair pathways.
KW - aging
KW - DNA repair
KW - Genomic instability
KW - interventions
KW - mitochondrial dysfunction
KW - replication stress
KW - transcription
U2 - 10.1016/B978-0-12-823761-8.00020-3
DO - 10.1016/B978-0-12-823761-8.00020-3
M3 - Book chapter
AN - SCOPUS:85142828328
SN - 978-0-12-823761-8
SP - 275
EP - 295
BT - Aging
A2 - Oliveira, Paulo J.
A2 - Malva, João O.
PB - Academic Press
ER -
ID: 332601098