Telomere and its role in the aging pathways: telomere shortening, cell senescence and mitochondria dysfunction

被引：177

作者：

Zhu, Yukun ^{[1
,2
]}

Liu, Xuewen ^{[1
,2
]}

Ding, Xuelu ^{[1
,2
]}

Wang, Fei ^{[3
]}

Geng, Xin ^{[1
,2
]}

机构：

[1] Tianjin Med Univ, Sch Basic Med Sci, Dept Biochem & Mol Biol, Tianjin 300070, Peoples R China

[2] Tianjin Med Univ, Minist Educ, Key Lab Immune Microenvironm & Dis, Tianjin 300070, Peoples R China

[3] Tianjin Med Univ, Gen Hosp, Dept Neurol, Tianjin 300052, Peoples R China

来源：

BIOGERONTOLOGY | 2019年 / 20卷 / 01期

关键词：

Telomere; Telomere shortening; Cellular senescence; Mitochondrial dysfunction; Aging; DNA-DAMAGE; MAMMALIAN TELOMERES; HOMOLOGOUS RECOMBINATION; SECRETORY PHENOTYPE; TISSUE HOMEOSTASIS; NEGATIVE REGULATOR; END-PROTECTION; QUADRUPLEX DNA; LIFE-SPAN; RNA;

D O I：

10.1007/s10522-018-9769-1

中图分类号：

R592 [老年病学]; C [社会科学总论];

学科分类号：

03 ; 0303 ; 100203 ;

摘要：

Aging is a biological process characterized by a progressive functional decline in tissues and organs, which eventually leads to mortality. Telomeres, the repetitive DNA repeat sequences at the end of linear eukaryotic chromosomes protecting chromosome ends from degradation and illegitimate recombination, play a crucial role in cell fate and aging. Due to the mechanism of replication, telomeres shorten as cells proliferate, which consequently contributes to cellular senescence and mitochondrial dysfunction. Cells are the basic unit of organismal structure and function, and mitochondria are the powerhouse and metabolic center of cells. Therefore, cellular senescence and mitochondrial dysfunction would result in tissue or organ degeneration and dysfunction followed by somatic aging through multiple pathways. In this review, we summarized the main mechanisms of cellular senescence, mitochondrial malfunction and aging triggered by telomere attrition. Understanding the molecular mechanisms involved in the aging process may elicit new strategies for improving health and extending lifespan.

引用

页码：1 / 16

页数：16

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