Evidence map›Paper›PMID 28289275›Full record

ArticleMolecular psychiatry2017

Epigenetic programming by stress and glucocorticoids along the human lifespan.

A S Zannas, G P Chrousos

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular psychiatry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
84citing papers in PubMed, 3 pooled it
7.3field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

84 citing papers in PubMed, 3 syntheses or guidelines pooled it, 153 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Trial
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  6. Review
  7. Review
  8. Acute stress induces changes in epigenome-wide DNA methylation.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
    Article
  9. Article
  10. Article
  11. Review
  12. The complicated relationship between inflammation and metabolic dysfunction.Journal of diabetes and metabolic disorders · 2025
    Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. The researcher's guide to selecting biomarkers in mental health studies.BioEssays : news and reviews in molecular, cellular and developmental biology · 2024
    Review
  18. Article
  19. Targeting Nr2e3 to Modulate Tet2 Expression: Therapeutic Potential for Depression Treatment.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
  20. Article

24 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 2 institutions in 3 countries.

A S ZannasDepartment of Translational Research in Psychiatry, Max Planck Institute of Psychiatry, Munich, Germany.
G P ChrousosFirst Department of Pediatrics and Division of Endocrinology, Metabolism and Diabetes, National and Kapodistrian University of Athens Medical School, Athens, Greece.
Max Planck Institute of Psychiatry · DENational and Kapodistrian University of Athens · GR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Psychosocial stress triggers a set of behavioral, neural, hormonal, and molecular responses that can be a driving force for survival when adaptive and time-limited, but may also contribute to a host of disease states if dysregulated or chronic. The beneficial or detrimental effects of stress are largely mediated by the hypothalamic-pituitary axis, a highly conserved neurohormonal cascade that culminates in systemic secretion of glucocorticoids. Glucocorticoids activate the glucocorticoid receptor, a ubiquitous nuclear receptor that not only causes widespread changes in transcriptional programs, but also induces lasting epigenetic modifications in many target tissues. While the epigenome remains sensitive to stressors throughout life, we propose two key principles that may govern the epigenetics of stress and glucocorticoids along the lifespan: first, the presence of distinct life periods, during which the epigenome shows heightened plasticity to stress exposure, such as in early development and at advanced age; and, second, the potential of stress-induced epigenetic changes to accumulate throughout life both in select chromatin regions and at the genome-wide level. These principles have important clinical and translational implications, and they show striking parallels with the existence of sensitive developmental periods and the cumulative impact of stressful experiences on the development of stress-related phenotypes. We hope that this conceptual mechanistic framework will stimulate fruitful research that aims at unraveling the molecular pathways through which our life stories sculpt genomic function to contribute to complex behavioral and somatic phenotypes.

Indexed as

AnimalsEpigenesis, GeneticGlucocorticoidsHumansReceptors, GlucocorticoidSignal TransductionStress, PsychologicalGlucocorticoidsReceptors, Glucocorticoid

Identifiers

PMID28289275
OpenAlexW2606520198

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.