Evidence map›Paper›PMID 29492295›Full record

ReviewEnvironmental epigenetics2016

Stress-induced transposon reactivation: a mediator or an estimator of allostatic load?

Daniel Nätt, Annika Thorsell

Open access · goldAbstract readReview
In one paragraph

Review in Environmental epigenetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.0field-weighted citation impact, top 12% 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

12 citing papers in PubMed, 27 citations in OpenAlex.

  1. A Quinoxaline 1,4-Dioxide Activates DNA Repair Systems inInternational journal of molecular sciences · 2025
    Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Can Early Life Stress Engender Biological Resilience?: Commentary.Journal of child & adolescent trauma · 2021
    Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Epigenetics in disease and well-being.Environmental epigenetics · 2016
    Article
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 1 institution in 1 country.

Daniel NättDepartment of Clinical and Experimental Medicine (IKE), Linkoping University, Center for Social and Affective Neuroscience (CSAN), Linkoping, Sweden.
Annika ThorsellDepartment of Clinical and Experimental Medicine (IKE), Linkoping University, Center for Social and Affective Neuroscience (CSAN), Linkoping, Sweden.
Linköping University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transposons are playing an important role in the evolution of eukaryotic genomes. These endogenous virus-like elements often amplify within their host genomes in a species specific manner. Today we have limited understanding when and how these amplification events happens. What we do know is that cells have evolved multiple line of defenses to keep these potentially invasive elements under control, often involving epigenetic mechanisms such as DNA-methylation and histone modifications. Emerging evidence shows a strong link between transposon activity and human aging and diseases, as well as a role for transposons in normal brain development. Controlling transposon activity may therefore uphold the fine balance between health and disease. In this article we investigate this balance, and sets it in relation to allostatic load, which conceptualize the link between stress and the "wear and tear" of the organism that leads to aging and disease. We hypothesize that stress-induced retrotransposon reactivation in humans may be used to estimate allostatic load, and may be a possible mechanism in which transposons amplify within species genomes.

Indexed as

allostasisallostatic loadepigenetic silencingretrotransposonsstresstransposons

Identifiers

PMID29492295
PMCPMC5804529
OpenAlexW2507292658

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.