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质疑端粒在衰老过程中的因果关系。

Questioning causal involvement of telomeres in aging.

作者信息

Simons Mirre J P

机构信息

Department of Animal and Plant Sciences, University of Sheffield, Sheffield S10 2TN, Sheffield, United Kingdom.

出版信息

Ageing Res Rev. 2015 Nov;24(Pt B):191-6. doi: 10.1016/j.arr.2015.08.002. Epub 2015 Aug 21.

Abstract

Multiple studies have demonstrated that telomere length predicts mortality and that telomeres shorten with age. Although rarely acknowledged these associations do not dictate causality. I review telomerase knockout and overexpression studies and find little support that telomeres cause aging. In addition, the causality hypothesis assumes that there is a critical telomere length at which senescence is induced. This generates the prediction that variance in telomere length decreases with age. In contrast, using meta-analysis of human data, I find no such decline. Inferring the causal involvement of telomeres in aging from current knowledge is therefore speculative and could hinder scientific progress.

摘要

多项研究表明,端粒长度可预测死亡率,且端粒会随着年龄增长而缩短。尽管这些关联很少被承认,但它们并不意味着存在因果关系。我回顾了端粒酶基因敲除和过表达研究,发现几乎没有证据支持端粒会导致衰老。此外,因果关系假说假定存在一个诱导衰老的关键端粒长度。这就产生了一个预测,即端粒长度的方差会随着年龄增长而减小。相比之下,通过对人类数据的荟萃分析,我并未发现这种下降。因此,从目前的知识推断端粒在衰老过程中的因果关系是推测性的,可能会阻碍科学进步。

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