Evidence map›Paper›PMID 19716833›Full record

ReviewToxicology and applied pharmacology2010

A systems biology perspective on Nrf2-mediated antioxidant response.

Qiang Zhang, Jingbo Pi, Courtney G Woods, Melvin E Andersen

Abstract readReview
In one paragraph

Review in Toxicology and applied pharmacology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
86citing papers in PubMed, 2 pooled it
–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

86 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Preventing Colitis-Associated Colon Cancer With Antioxidants: A Systematic Review.Cellular and molecular gastroenterology and hepatology · 2021
    Pooled it
  3. Trial
  4. Trial
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Anti-Wrinkling Effect of 3,4,5-tri-Antioxidants (Basel, Switzerland) · 2023
    Article
  13. Article
  14. Article
  15. Propofol Induces the Expression of Nrf2 and HO-1 inTropical medicine and infectious disease · 2023
    Article
  16. Article
  17. Review
  18. Inflammatory bowel disease and carcinogenesis.Cancer metastasis reviews · 2022
    Review
  19. Article
  20. Article

26 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

4 authors.

Qiang ZhangDivision of Computational Biology, The Hamner Institutes for Health Sciences, 6 Davis Drive, Research Triangle Park, NC 27709, USA. qzhang@thehamner.org
Jingbo Pi
Courtney G Woods
Melvin E Andersen

Funding

VOLATILE ORGANIC CONTAMINANTS--QUANTIFYING THEIR MOVEMENT IN THE UNSATURATED ZONEP42ES004911 · NIEHS · MICHIGAN STATE UNIVERSITY · PI Timothy R. Zacharewski · 1989 to 2026
$64.9M
Paradoxical roles of Nrf2 activation in arsenic-induced beta-cell dysfunctionR01ES016005 · NIEHS · THE HAMNER INSTITUTES · PI PI, JINGBO · 2008 to 2012
$2.5M
NIEHS NIH HHS P42 ES004911NIEHS NIH HHS P42ES04911NIEHS NIH HHS R01 ES016005NIEHS NIH HHS R01ES016005
6 · The paper itself

Abstract

Cells in vivo are constantly exposed to reactive oxygen species (ROS) generated endogenously and exogenously. To defend against the deleterious consequences of ROS, cells contain multiple antioxidant enzymes expressed in various cellular compartments to scavenge these toxic species. Under oxidative stresses, these antioxidant enzymes are upregulated to restore redox homeostasis. Such an adaptive response results from the activation of a redox-sensitive gene regulatory network mediated by nuclear factor E2-related factor 2. To more completely understand how the redox control system is designed by nature to meet homeostatic goals, we have examined the network from a systems perspective using engineering approaches. As with man-made control devices, the redox control system can be decomposed into distinct functional modules, including transducer, controller, actuator, and plant. Cells achieve specific performance objectives by utilizing nested feedback loops, feedforward control, and ultrasensitive signaling motifs, etc. Given that endogenously generated ROS are also used as signaling molecules, our analysis suggests a novel mode of action to explain oxidative stress-induced pathological conditions and diseases. Specifically, by adaptively upregulating antioxidant enzymes, oxidative stress may inadvertently attenuate ROS signals that mediate physiological processes, resulting in aberrations of cellular functions and adverse consequences. Lastly, by simultaneously considering the two competing cellular tasks-adaptive antioxidant defense and ROS signaling-we re-examine the premise that dietary antioxidant supplements is generally beneficial to human health. Our analysis highlights some possible adverse effects of these widely consumed antioxidants.

Indexed as

Oxidative StressSignal TransductionSystems BiologyAnimalsAntioxidantsHomeostasisHumansNF-E2-Related Factor 2Oxidation-ReductionReactive Oxygen SpeciesAntioxidantsNF-E2-Related Factor 2Reactive Oxygen Species

Identifiers

PMID19716833
PMCPMC2837757

What OpenQuestion holds

Textmetadata
LicenceTDM
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.