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Could Telomere Length and Lifespan be Enhanced with CRISPR?

Could Telomere Length and Lifespan be Enhanced with CRISPR?

Image credit: Thomas Ried/NCI Center for Cancer Research

By Jamila Ahmed on Jul 28, 2020

Could CRISPR editing be used to improve lifespan by enhancing telomere length?

Previous research suggests that maintaining telomere length can reverse age-related diseases and may improve lifespan, as TERT overexpression in mice delayed aging and enhanced life [1]expectancy. Furthermore, a vector containing TERT improved the lifespan of one-year old and two-year old mice by 24% and 13% [2]respectively. The use of CRISPR-Cas in telomeres for aging research is a largely unexplored area. In one study, the TERT promoter was targeted by CRISPR-Cas to vary the gene expression of TERT, some mutations had increased telomerase levels similar to that seen in the immortalised [3]cells. In the future, studies using CRISPR editing to modify the TERT, TERC, or TRF1 genes should be conducted to assess the effect on lifespan.

Interestingly, DNA methyltransferase 2 deficient cells have shortened telomeres and decreased telomerase [4]activity. Therefore, exploring the use of epigenome editing could be ground-breaking in the anti-aging field. Specifically, epigenetic editing of the TERT gene could be conducted to observe its effect on lifespan.


[1] Tomás-Loba, Antonia, et al. "Telomerase reverse transcriptase delays aging in cancer-resistant mice." Cell, 135.4, 2008, pp. 609-622.

[2] de Jesus, Bruno Bernardes, et al. "Telomerase gene therapy in adult and old mice delays aging and increases longevity without increasing cancer." EMBO molecular medicine, 4.8, 2012, pp. 691-704.

[3] Chiba, Kunitoshi, et al. "Cancer-associated TERT promoter mutations abrogate telomerase silencing." Elife, 4, 2015, pp. e07918.

[4] Lewinska, Anna, et al. "Downregulation of methyltransferase Dnmt2 results in condition‐dependent telomere shortening and senescence or apoptosis in mouse fibroblasts." Journal of cellular physiology, 232.12, 2017, pp. 3714-3726.

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