DNA methylation-based biomarkers and the epigenetic clock theory of ageing

被引：1828

作者：

Horvath, Steve ^{[1
,2
]}

Raj, Kenneth ^{[3
]}

机构：

[1] David Geffen Sch Med, Gonda Res Ctr, Dept Human Genet, Los Angeles, CA 90095 USA

[2] Univ Calif Los Angeles, Sch Publ Hlth, Dept Biostat, Los Angeles, CA 90024 USA

[3] Publ Hlth England, Ctr Radiat Chem & Environm Hazards, Radiat Effects Dept, Chilton, Didcot, England

来源：

NATURE REVIEWS GENETICS | 2018年 / 19卷 / 06期

关键词：

ALL-CAUSE MORTALITY; TELOMERE LENGTH; CELLULAR SENESCENCE; BIOLOGICAL AGE; GENOME-WIDE; CHRONOLOGICAL AGE; STEM-CELLS; CROSS-TALK; CANCER; DISEASE;

D O I：

10.1038/s41576-018-0004-3

中图分类号：

Q3 [遗传学];

学科分类号：

071007 ; 090102 ;

摘要：

Identifying and validating molecular targets of interventions that extend the human health span and lifespan has been difficult, as most clinical biomarkers are not sufficiently representative of the fundamental mechanisms of ageing to serve as their indicators. In a recent breakthrough, biomarkers of ageing based on DNA methylation data have enabled accurate age estimates for any tissue across the entire life course. These 'epigenetic clocks' link developmental and maintenance processes to biological ageing, giving rise to a unified theory of life course. Epigenetic biomarkers may help to address long-standing questions in many fields, including the central question: why do we age?

引用

页码：371 / 384

页数：14

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