English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Environmental stress is ubiquitous in modern societies and can exert a profound and cumulative impact on cell function and health phenotypes. This impact is thought to be in large part mediated by the action of glucocorticoid stress hormones, primarily cortisol in humans. While the underlying molecular mechanisms are unclear, epigenetics-the chemical changes that regulate genomic function without altering the genetic code-has emerged as a key link between environmental exposures and phenotypic outcomes. The present study assessed genome-wide DNA (CpG) methylation, one of the key epigenetic mechanisms, at three timepoints during prolonged (51-day) exposure of cultured human fibroblasts to naturalistic cortisol levels, which can be reached in human tissues during in vivo stress. The findings support a spatiotemporal model of profound and widespread stress hormone-driven methylomic changes that emerge at selected CpG sites, are more likely to spread to nearby located CpGs, and quantitatively accrue at open sea, glucocorticoid receptor binding, and chromatin-accessible sites. Taken together, these findings provide novel insights into how prolonged stress may impact the epigenome, with potentially important implications for stress-related phenotypes.

Naturalistic Stress Hormone Levels Drive Cumulative Epigenomic Changes along the Cellular Lifespan