Cellular senescence and premature aging in Down Syndrome

被引：11

作者：

Peng, Lianli ^{[1
]}

Baradar, Alireza A. ^{[1
]}

Aguado, Julio ^{[1
]}

Wolvetang, Ernst ^{[1
]}

机构：

[1] Univ Queensland, Australian Inst Biotechnol & Nanotechnol, St Lucia, Qld 4072, Australia

来源：

MECHANISMS OF AGEING AND DEVELOPMENT | 2023年 / 212卷

关键词：

Cellular senescence; Down syndrome; Premature aging; OXIDATIVE STRESS; MITOCHONDRIAL DYSFUNCTION; GENE-EXPRESSION; DNA-DAMAGE; TELOMERE LENGTH; MOUSE MODEL; IN-VIVO; CHROMOSOME-21; PROLIFERATION; ACTIVATION;

D O I：

10.1016/j.mad.2023.111824

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Down syndrome (DS) is a genetic disorder caused by an extra copy of chromosome 21, resulting in cognitive impairment, physical abnormalities, and an increased risk of age-related co-morbidities. Individuals with DS exhibit accelerated aging, which has been attributed to several cellular mechanisms, including cellular senescence, a state of irreversible cell cycle arrest that is associated with aging and age-related diseases. Emerging evidence suggests that cellular senescence may play a key role in the pathogenesis of DS and the development of age-related disorders in this population. Importantly, cellular senescence may be a potential therapeutic target in alleviating age-related DS pathology. Here, we discuss the importance of focusing on cellular senescence to understand accelerated aging in DS. We review the current state of knowledge regarding cellular senescence and other hallmarks of aging in DS, including its putative contribution to cognitive impairment, multi-organ dysfunction, and premature aging phenotypes.

引用

页数：9

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