Evidence map›Paper›PMID 28667066›Full record

ReviewClinical science (London, England : 1979)2017

Redox theory of aging: implications for health and disease.

Young-Mi Go, Dean P Jones

Open access · bronzeAbstract readReview
In one paragraph

Review in Clinical science (London, England : 1979), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
90citing papers in PubMed, 1 pooled it
11.3field-weighted citation impact, top 1% 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

90 citing papers in PubMed, 1 synthesis or guideline pooled it, 171 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Article
  5. Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Changes in the brain [NADFrontiers in aging neuroscience · 2026
    Review
  12. Review
  13. Review
  14. Article
  15. Review
  16. Review
  17. Review
  18. Redox organization of living systems.Free radical biology & medicine · 2024
    Review
  19. Article
  20. Review

30 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 1 institution in 1 country.

Young-Mi GoDivision of Pulmonary Medicine, Department of Medicine, Emory University, Atlanta, GA 30322, U.S.A.
Dean P JonesDivision of Pulmonary Medicine, Department of Medicine, Emory University, Atlanta, GA 30322, U.S.A. dpjones@emory.edu.
Emory University · US

Funding

Pilot Project ProgramP30ES019776 · NIEHS · EMORY UNIVERSITY · PI William Michael Caudle · 2013 to 2026
$22.6M
Cytoplasmic-nuclear redox signaling: Disruption by dietary cadmium levelsR01ES023485 · NIEHS · EMORY UNIVERSITY · PI GO KANG, YOUNG-MI, JONES, DEAN PAUL · 2014 to 2018
$1.8M
Orbitrap Elite/H-ESI BundleS10OD018006 · OD · EMORY UNIVERSITY · PI JONES, DEAN PAUL · 2014 to 2014
$600k
Mitochondria Environmental Stress Signaling NetworksR21ES025632 · NIEHS · EMORY UNIVERSITY · PI GO KANG, YOUNG-MI, JONES, DEAN PAUL · 2015 to 2017
$576k
NIEHS NIH HHS P30 ES019776NIEHS NIH HHS R01 ES023485NIEHS NIH HHS R21 ES025632NIH HHS S10 OD018006
6 · The paper itself

Abstract

Genetics ultimately defines an individual, yet the phenotype of an adult is extensively determined by the sequence of lifelong exposures, termed the exposome. The redox theory of aging recognizes that animals evolved within an oxygen-rich environment, which created a critical redox interface between an organism and its environment. Advances in redox biology show that redox elements are present throughout metabolic and structural systems and operate as functional networks to support the genome in adaptation to environmental resources and challenges during lifespan. These principles emphasize that physical and functional phenotypes of an adult are determined by gene-environment interactions from early life onward. The principles highlight the critical nature of cumulative exposure memories in defining changes in resilience progressively during life. Both plasma glutathione and cysteine systems become oxidized with aging, and the recent finding that cystine to glutathione ratio in human plasma predicts death in coronary artery disease (CAD) patients suggests this could provide a way to measure resilience of redox networks in aging and disease. The emerging concepts of cumulative gene-environment interactions warrant focused efforts to elucidate central mechanisms by which exposure memory governs health and etiology, onset and progression of disease.

Indexed as

Oxidation-ReductionAgingBiomarkersCoronary Artery DiseaseGene-Environment InteractionGlutathioneHumansMetalsModels, BiologicalOxidative StressRegenerative MedicineSalivary CystatinsBiomarkersCST4 protein, humanGlutathioneMetalsSalivary Cystatinsdisease preventionEarly life exposurehealthy longevitypersonalized medicineplasma thiol and disulfidesequencing human exposome

Identifiers

PMID28667066
PMCPMC5773128
OpenAlexW2732353044

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.