{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,12]],"date-time":"2026-06-12T01:38:58Z","timestamp":1781228338226,"version":"3.54.1"},"reference-count":29,"publisher":"MDPI AG","issue":"12","license":[{"start":{"date-parts":[[2020,11,27]],"date-time":"2020-11-27T00:00:00Z","timestamp":1606435200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Genes"],"abstract":"<jats:p>Psychosocial stress, especially when chronic or excessive, can increase disease risk and accelerate biological aging. Although the underlying mechanisms are unclear, in vivo studies have associated exposure to stress and glucocorticoid stress hormones with shorter telomere length. However, the extent to which prolonged glucocorticoid exposure can shorten telomeres in controlled experimental settings remains unknown. Using a well-characterized cell line of human fibroblasts that undergo gradual telomere shortening during serial passaging in culture, we show that prolonged exposure (up to 51 days) to either naturalistic levels of the human endogenous glucocorticoid cortisol or the more potent synthetic glucocorticoid dexamethasone is not sufficient to accelerate telomere shortening. While our findings await extension in other cell types and biological contexts, they indicate that the in vivo association of psychosocial stress with telomere shortening is unlikely to be mediated by a direct and universal glucocorticoid effect on telomere length.<\/jats:p>","DOI":"10.3390\/genes11121425","type":"journal-article","created":{"date-parts":[[2020,11,28]],"date-time":"2020-11-28T03:51:16Z","timestamp":1606535476000},"page":"1425","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":12,"title":["Prolonged Glucocorticoid Exposure Does Not Accelerate Telomere Shortening in Cultured Human Fibroblasts"],"prefix":"10.3390","volume":"11","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6897-9652","authenticated-orcid":false,"given":"Anthony S.","family":"Zannas","sequence":"first","affiliation":[{"name":"Department of Psychiatry, University of North Carolina, Chapel Hill, NC 27599, USA"},{"name":"Department of Genetics, University of North Carolina, Chapel Hill, NC 27514, USA"},{"name":"Department of Psychiatry and Behavioral Sciences, Duke University Medical Center, Durham, NC 27710, USA"},{"name":"Carolina Stress Initiative, University of North Carolina School of Medicine, Chapel Hill, NC 27514, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Oksana","family":"Kosyk","sequence":"additional","affiliation":[{"name":"Department of Psychiatry, University of North Carolina, Chapel Hill, NC 27599, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Calvin S.","family":"Leung","sequence":"additional","affiliation":[{"name":"Department of Psychiatry, University of North Carolina, Chapel Hill, NC 27599, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2020,11,27]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"389","DOI":"10.31887\/DCNS.2019.21.4\/azannas","article-title":"Epigenetics as a Key Link between Psychosocial Stress and Aging: Concepts, Evidence, Mechanisms","volume":"21","author":"Zannas","year":"2019","journal-title":"Dialogues Clin. 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