Evidence map›Paper›PMID 25462060›Full record

ReviewRedox biology2014

Regulation of the effects of CYP2E1-induced oxidative stress by JNK signaling.

Jörn M Schattenberg, Mark J Czaja

Open access · goldAbstract readReview
In one paragraph

Review in Redox biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed, 1 pooled it
4.2field-weighted citation impact, top 6% 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

46 citing papers in PubMed, 1 synthesis or guideline pooled it, 93 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Synergistic toxicity in alcohol-associated liver disease and PFAS exposure.Toxicological sciences : an official journal of the Society of Toxicology · 2025
    Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Lipid nanoparticle delivery of siRNA targetingZhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2023
    Article
  20. Review
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 2 countries.

Jörn M SchattenbergI. Department of Medicine, University Medical Center of the Johannes Gutenberg University, 55131 Mainz, Germany.
Mark J CzajaDepartment of Medicine and Marion Bessin Liver Research Center, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, USA. Electronic address: mark.czaja@einstein.yu.edu.
Albert Einstein College of Medicine · USJohannes Gutenberg University Mainz · DE

Funding

Special Animal CoreP30DK041296 · NIDDK · YESHIVA UNIVERSITY · PI WOLKOFF, ALLAN W · 1989 to 2018
$22.9M
MODULATION OF ACUTE TOXIC LIVER INJURYR01DK044234 · NIDDK · YESHIVA UNIVERSITY · PI SRINIVASAN, SHANTHI K · 1992 to 2023
$7.6M
Role of CYP2E1 in the Progression to NASHR01DK061498 · NIDDK · YESHIVA UNIVERSITY · PI CZAJA, MARK J · 2002 to 2015
$4.7M
Regulation of the innate immune response in alcoholic liver disease by autophagyR01AA022601 · NIAAA · EMORY UNIVERSITY · PI CZAJA, MARK J · 2014 to 2018
$2.1M
NIAAA NIH HHS R01 AA022601NIAAA NIH HHS R01AA022601NIDDK NIH HHS P30 DK041296NIDDK NIH HHS R01 DK044234NIDDK NIH HHS R01DK044234NIDDK NIH HHS R01 DK061498NIDDK NIH HHS R01DK061498
6 · The paper itself

Abstract

The generation of excessive amounts of reactive oxygen species (ROS) leads to cellular oxidative stress that underlies a variety of forms of hepatocyte injury and death including that from alcohol. Although ROS can induce cell damage through direct effects on cellular macromolecules, the injurious effects of ROS are mediated largely through changes in signal transduction pathways such as the mitogen-activated protein kinase c-Jun N-terminal kinase (JNK). In response to alcohol, hepatocytes have increased levels of the enzyme cytochrome P450 2E1 (CYP2E1) which generates an oxidant stress that promotes the development of alcoholic steatosis and liver injury. These effects are mediated in large part through overactivation of JNK that alters cell death pathways. Targeting the JNK pathway or its downstream effectors may be a useful therapeutic approach to the oxidative stress generated by CYP2E1 in alcoholic liver disease.

Indexed as

MAP Kinase Signaling SystemOxidative StressAnimalsCell DeathCytochrome P-450 CYP2E1Fatty LiverHumansJNK Mitogen-Activated Protein KinasesLiverMolecular Targeted TherapyReactive Oxygen SpeciesCytochrome P-450 CYP2E1JNK Mitogen-Activated Protein KinasesReactive Oxygen SpeciesAlcoholic liver diseasec-Jun N-terminal kinaseCytochrome P450 2E1Mitogen-activated protein kinasesOxidative stress

Identifiers

PMID25462060
PMCPMC4218941
OpenAlexW2041020444

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.