Evidence map›Paper›PMID 20919933›Full record

ReviewAntioxidants & redox signaling2011

The redox basis of epigenetic modifications: from mechanisms to functional consequences.

Anthony R Cyr, Frederick E Domann

Abstract readReview
In one paragraph

Review in Antioxidants & redox signaling, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 140 papers.

0numbers the graph read from it
0cells of the map it votes in
140citing papers in PubMed
–field-weighted citation impact
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

140 citing papers in PubMed.

  1. Trial
  2. Article
  3. Review
  4. Review
  5. Review
  6. Review
  7. Review
  8. Fumonisin BEpigenetics · 2025
    Article
  9. Article
  10. Article
  11. Article
  12. Overview of Oxidative Stress in Systemic Lupus Erythematosus.Antioxidants (Basel, Switzerland) · 2025
    Review
  13. Potential promising of synthetic lethality in cancer research and treatment.Naunyn-Schmiedeberg's archives of pharmacology · 2025
    Review
  14. Review
  15. Review
  16. Review
  17. Article
  18. Review
  19. Article
  20. Article

80 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.

Anthony R CyrFree Radical and Radiation Biology Program, Department of Radiation Oncology, Carver College of Medicine, The University of Iowa, Iowa City, Iowa 52242-1181, USA.
Frederick E Domann

Funding

MEDICAL SCIENTIST TRAINING PROGRAMT32GM007337 · NIGMS · UNIVERSITY OF IOWA · PI GEYER, PAMELA K., LENTZ, STEVEN R · 1985 to 2020
$15.9M
TRAINING PROGRAM IN FREE RADICAL AND RADIATION BIOLOGYT32CA078586 · NCI · UNIVERSITY OF IOWA · PI SPITZ, DOUGLAS ROBERT · 1999 to 2024
$5.7M
Epigenetic factors governing SOD2 gene expressionR01CA073612 · NCI · UNIVERSITY OF IOWA · PI DOMANN, FREDERICK E · 2003 to 2007
$1.3M
Molecular Species Responsible for Tumor Supressive Effect of MnSODR01CA115438 · NCI · UNIVERSITY OF IOWA · PI DOMANN, FREDERICK E · 2007 to 2011
$1.2M
NCI NIH HHS R01 CA073612NCI NIH HHS R01CA073612NCI NIH HHS R01 CA115438NCI NIH HHS R01CA115438NCI NIH HHS T32CA078586NIGMS NIH HHS T32 GM007337
6 · The paper itself

Abstract

Epigenetic modifications represent mechanisms by which cells may effectively translate multiple signaling inputs into phenotypic outputs. Recent research is revealing that redox metabolism is an increasingly important determinant of epigenetic control that may have significant ramifications in both human health and disease. Numerous characterized epigenetic marks, including histone methylation, acetylation, and ADP-ribosylation, as well as DNA methylation, have direct linkages to central metabolism through critical redox intermediates such as NAD(+), S-adenosyl methionine, and 2-oxoglutarate. Fluctuations in these intermediates caused by both normal and pathologic stimuli may thus have direct effects on epigenetic signaling that lead to measurable changes in gene expression. In this comprehensive review, we present surveys of both metabolism-sensitive epigenetic enzymes and the metabolic processes that may play a role in their regulation. To close, we provide a series of clinically relevant illustrations of the communication between metabolism and epigenetics in the pathogenesis of cardiovascular disease, Alzheimer disease, cancer, and environmental toxicity. We anticipate that the regulatory mechanisms described herein will play an increasingly large role in our understanding of human health and disease as epigenetics research progresses.

Indexed as

Epigenesis, GeneticAcetylationAnimalsHumansMethylationOxidation-Reduction

Identifiers

PMID20919933
PMCPMC3118659

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.