STING deficiency does not rescue short telomere-mediated aging phenotypes and longevity in TERC- or TERT-telomerase deficient mice.

Authors

Rosa M Marión, José Carlos González, Juana M Flores, Elena Piñeiro-Yáñez, Rosa Serrano, Maria A Blasco

Published in

Cell reports. Volume 45. Issue 8. Pages 117786. Aug 06, 2026. Epub Aug 06, 2026.

Abstract

The cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) pathway plays a key role in responding to viral genomes and endogenous DNA byproducts by inducing inflammatory pathways. Its roles in senescence and in the response to telomere shortening have also recently been proposed. To address its role in age-related pathologies and decreased longevity associated with short telomeres, we generated double-mutant mice deficient for STING and either the telomerase RNA component (TERC) or the telomerase reverse transcriptase (TERT) component. In both telomerase-deficient mouse cohorts, STING deficiency did not rescue any major phenotypes, including decreased body weight, infertility, multiple degenerative pathologies and, importantly, the progressively decreased maximum and median lifespan of increasing generations of Terc- or Tert-deficient mice. These findings indicate that STING does not mediate aging phenotypes associated with short telomeres in mammals. Furthermore, they have potential relevance for therapeutic strategies based on STING inhibition in short-telomere-associated age-related diseases in mammalian organisms.

PMID:
42560816
Bibliographic data and abstract were imported from PubMed on 07 Aug 2026.

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