The emerging role of alternative splicing in senescence and aging

被引：124

作者：

Deschenes, Mathieu ^{[1
]}

Chabot, Benoit ^{[1
]}

机构：

[1] Univ Sherbrooke, Dept Microbiol & Infect Dis, Fac Med & Hlth Sci, Sherbrooke, PQ J1E 4K8, Canada

来源：

AGING CELL | 2017年 / 16卷 / 05期

基金：

加拿大健康研究院;

关键词：

aging; alternative splicing; pre-mRNA; RNA; RNA binding proteins; senescence; splice variants; splicing; GROWTH-FACTOR-I; EXTENDS LIFE-SPAN; GILFORD PROGERIA SYNDROME; TUMOR-SUPPRESSOR ING1; E PEPTIDE ACTIONS; TELOMERE DYSFUNCTION; CELLULAR SENESCENCE; DNA-DAMAGE; IGF-I; SKELETAL-MUSCLE;

D O I：

10.1111/acel.12646

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Deregulation of precursor mRNA splicing is associated with many illnesses and has been linked to age-related chronic diseases. Here we review recent progress documenting how defects in the machinery that performs intron removal and controls splice site selection contribute to cellular senescence and organismal aging. We discuss the functional association linking p53, IGF-1, SIRT1, and ING-1 splice variants with senescence and aging, and review a selection of splicing defects occurring in accelerated aging (progeria), vascular aging, and Alzheimer's disease. Overall, it is becoming increasingly clear that changes in the activity of splicing factors and in the production of key splice variants can impact cellular senescence and the aging phenotype.

引用

页码：918 / 933

页数：16

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