ArticlePsychoneuroendocrinology2023
Maximal telomerase activity capacity (mTAC) underlies the link between the cortisol response to stress and telomere length.
Article in Psychoneuroendocrinology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 4 citations in OpenAlex.
- Maternal health behavior during pregnancy mediates the relationship between maternal stress and newborn telomere length.Brain, behavior, & immunity - health · 2026Article
- Age and gender intersectionality among African Americans: Salivary uric acid is associated with shorter telomere length in younger adults and men.Psychoneuroendocrinology · 2025Article
- Associations of family affluence with cortisol production and telomere length in European children.EBioMedicine · 2025Article
- Stress and telomere length in leukocytes: Investigating the role of GABRA6 gene polymorphism and cortisol.Psychoneuroendocrinology · 2025Article
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 4 countries.
Funding
Abstract
Exposure to various forms of stress has been associated with shorter telomere length (TL). However, the molecular underpinnings of this effect are poorly understood. Based on an understanding of the key role of the reverse transcriptase enzyme telomerase in regulating TL, and building upon our previous work in developing and validating a biomarker of the capacity of cells to express telomerase (maximal telomerase activity capacity (mTAC)), we examine here the hypotheses that mTAC is positively associated with TL and that the effect of stress on TL is mediated by individual differences in mTAC. In a proof-of-principle study of 28 healthy women and men we quantified the cortisol response to a standardized stress challenge, the Trier Social Stress Test (TSST), and we concurrently assessed peripheral blood mononuclear cell (PBMC) mTAC and TL. Our results indicated that higher mTAC levels were associated with longer TL (r = 0.50, p = .01). Moreover, mediational analysis suggested that the effect of the cortisol stress response on TL was mediated by mTAC (completely standardized β = -0.17, bootstrap CI95 %: -0.44 to -0.01). Thus, our findings support the premise that individual differences in the capacity of cells to up-regulate telomerase may represent a key mediator in the link between stress and TL.
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Registered trials
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