Questioning causal involvement of telomeres in aging
Questioning causal involvement of telomeres in aging
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DOI：
10.1016/j.arr.2015.08.002
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发表时间：
2015-11
影响因子：
13.1
通讯作者：
M. Simons
中科院分区：
文献类型：
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作者：
M. Simons
多项研究表明，端粒长度可以预测死亡率，而端粒长度会随着年龄的增长而缩短。尽管很少有人承认，但这些关联并不决定因果关系。我回顾了端粒酶基因敲除和过度表达的研究，发现几乎没有支持端粒导致衰老的证据。此外，因果关系假说假定有一个诱导衰老的临界端粒长度。这就产生了这样一种预测，即端粒长度的差异随着年龄的增长而减少。相比之下，使用人类数据的荟萃分析，我发现没有这样的下降。因此，从目前的知识推断端粒与衰老的因果关系是一种推测，可能会阻碍科学进步。
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.