Evidence map›Paper›PMID 29194686›Full record

ReviewHepatology (Baltimore, Md.)2018

New insights into the role and mechanism of c-Jun-N-terminal kinase signaling in the pathobiology of liver diseases.

Sanda Win, Tin Aung Than, Jun Zhang, Christina Oo, Robert Win Maw Min, Neil Kaplowitz

Open access · bronzeAbstract readReview
In one paragraph

Review in Hepatology (Baltimore, Md.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
91citing papers in PubMed, 1 pooled it
5.9field-weighted citation impact, top 3% 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

91 citing papers in PubMed, 1 synthesis or guideline pooled it, 168 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Antioxidants (Basel, Switzerland) · 2026
    Article
  5. The E3 Ligase RNF8 Promotes Ubiquitination and Degradation of ChREBPα During Liver Stress Response.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. NovelCurrent organic synthesis · 2025
    Article
  16. Article
  17. Hepatoprotective effects ofIranian journal of basic medical sciences · 2025
    Article
  18. Article
  19. Review
  20. Article

31 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

6 authors at 1 institution in 1 country.

Sanda WinUSC Research Center for Liver Disease, Department of Medicine, Keck School of Medicine of USC, Los Angeles, CA.ORCID 0000-0001-7694-5172
Tin Aung ThanUSC Research Center for Liver Disease, Department of Medicine, Keck School of Medicine of USC, Los Angeles, CA.
Jun ZhangUSC Research Center for Liver Disease, Department of Medicine, Keck School of Medicine of USC, Los Angeles, CA.
Christina OoUSC Research Center for Liver Disease, Department of Medicine, Keck School of Medicine of USC, Los Angeles, CA.
Robert Win Maw MinUSC Research Center for Liver Disease, Department of Medicine, Keck School of Medicine of USC, Los Angeles, CA.
Neil KaplowitzUSC Research Center for Liver Disease, Department of Medicine, Keck School of Medicine of USC, Los Angeles, CA.
Keck Hospital of USC · US

Funding

USC RESEARCH CENTER FOR LIVER DISEASES: PILOT PROGRAMSP30DK048522 · NIDDK · UNIVERSITY OF SOUTHERN CALIFORNIA · PI KAPLOWITZ, NEIL · 1995 to 2020
$21.8M
Role of Glutathione Redox Status in HepatotoxicityR01DK067215 · NIDDK · UNIVERSITY OF SOUTHERN CALIFORNIA · PI KAPLOWITZ, NEIL · 2005 to 2019
$5.6M
NIDDK NIH HHS P30 DK048522NIDDK NIH HHS R01 DK067215
6 · The paper itself

Abstract

The c-Jun-N-terminal-kinase (JNK) family is highly conserved across species such as Drosophila, C. elegans, zebrafish and mammals, and plays a central role in hepatic physiologic and pathophysiologic responses. These responses range from cell death to cell proliferation and carcinogenesis, as well as metabolism and survival, depending on the specific context and duration of activation of the JNK signaling pathway. Recently, several investigators identified the key molecules in the JNK activation loop which include apoptosis signal-regulating kinase (ASK1) and SH3-domain binding protein 5 (Sab) and their involvement in acute or chronic liver disease models. Thus, regulating JNK activation through modulating the JNK activation loop may represent an important new strategy in the prevention and treatment of acute and chronic liver diseases. In this review, we will discuss the molecular pathophysiology of the JNK activation loop and its role in the pathogenesis of liver diseases. (Hepatology 2018;67:2013-2024).

Indexed as

AnimalsCell DeathCell ProliferationHumansJNK Mitogen-Activated Protein KinasesLiverLiver DiseasesMAP Kinase Signaling SystemJNK Mitogen-Activated Protein Kinases

Identifiers

PMID29194686
PMCPMC5906137
OpenAlexW2772781313

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.