Evidence map›Paper›PMID 19642868›Full record

ReviewBiological chemistry2009

Mechanisms of liver disease: cross-talk between the NF-kappaB and JNK pathways.

Salvatore Papa, Concetta Bubici, Francesca Zazzeroni, Guido Franzoso

Open access · greenAbstract readReview
In one paragraph

Review in Biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed, 2 pooled it
3.0field-weighted citation impact, top 9% 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

77 citing papers in PubMed, 2 syntheses or guidelines pooled it, 152 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. New Insights into the Role of NF-κB in Hepatitis B Virus Infection.International journal of biological sciences · 2026
    Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. Association betweenWorld journal of hepatology · 2025
    Article
  15. An Nrf2-NF-κB Crosstalk Controls Hepatocyte Proliferation in the Normal and Injured Liver.Cellular and molecular gastroenterology and hepatology · 2025
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

17 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 at 2 institutions in 2 countries.

Salvatore PapaDepartment of Immunology, Investigative Science, Imperial College London, London W12 0NN, UK. s.papa@imperial.ac.uk
Concetta Bubici
Francesca Zazzeroni
Guido Franzoso
Imperial College London · GBUniversity of L'Aquila · IT

Funding

The NF-kB Target, Gadd45Beta, in Lymphocytes and LiverR01CA084040 · NCI · UNIVERSITY OF CHICAGO · PI FRANZOSO, GUIDO · 2000 to 2009
$2.6M
Gadd45beta in JNK Signaling, Apoptosis, and CancerR01CA098583 · NCI · UNIVERSITY OF CHICAGO · PI FRANZOSO, GUIDO · 2003 to 2007
$1.5M
Cancer Research UK C26587-A8839NCI NIH HHS CA84040NCI NIH HHS CA98583NCI NIH HHS R01 CA084040NCI NIH HHS R01 CA098583
6 · The paper itself

Abstract

The liver plays a central role in the transformation and degradation of endogenous and exogenous chemicals, and in the removal of unwanted cells such as damaged, genetically mutated and virus-infected cells. Because of this function, the liver is susceptible to toxicity caused by the products generated during these natural occurrences. Hepatocyte death is the major feature of liver injury. In response to liver injury, specific intracellular processes are initiated to maintain liver integrity. Inflammatory cytokines including tumor necrosis factor (TNF)alpha and interleukin-6 (IL-6) are key mediators of these processes and activate different cellular response such as proliferation, survival and death. TNFalpha induces specific signaling pathways in hepatocytes that lead to activation of either pro-survival mediators or effectors of cell death. Whereas activation of transcription factor NF-kappaB promotes survival, c-Jun N-terminal kinases (JNKs) and caspases are strategic effectors of cell death in the TNFalpha-mediated signaling pathway. This review summarizes recent advances in the mechanisms of TNFalpha-induced hepatotoxicity and suggests that NF-kappaB plays a protective role against JNK-induced hepatocyte death. Identification of the mechanisms regulating interplay between the NF-kappaB and JNK pathways is required in the search for novel targets for the treatment of liver disease, including hepatitis and hepatocellular carcinoma.

Indexed as

AnimalsCarcinoma, HepatocellularCell Physiological PhenomenaHepatitisHumansJNK Mitogen-Activated Protein KinasesLiver DiseasesNF-kappa BSignal TransductionJNK Mitogen-Activated Protein KinasesNF-kappa B

Identifiers

PMID19642868
PMCPMC2775491
OpenAlexW110144856

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.