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

Papa, Salvatore; Bubici, Concetta; Zazzeroni, Francesca; Franzoso, Guido

doi:10.1515/bc.2009.111

Cited by 156Liver physiology and pathologyDrug-Induced Hepatotoxicity and ProtectionNF-κB Signaling Pathways

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

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Papa, Salvatore, Bubici, Concetta, Zazzeroni, Francesca, Franzoso, Guido·2009·bchm

DOI 10.1515/bc.2009.111PMC PMC2775491

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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.

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NF-κB inhibits hepatocyte apoptosis and accelerates liver regeneration by promoting pro-survival and anti-apoptotic genes.
“Studies have demonstrated that NF-κB inhibits hepatocyte apoptosis and accelerates LR by promoting the expression of pro-survival and anti-apoptotic genes[54].”
From Liver regeneration after partial hepatectomy: Triggers and mechanisms (2025) · cites this paper as [54]
The Introduction says NF-κB protects hepatocytes from apoptosis through expression of anti-apoptotic genes, and the ‘NF-κB in liver regeneration’ section reports a role in hepatocyte survival and proliferation after partial hepatectomy. It does not establish that NF-κB accelerates liver regeneration through those genes; that section also notes a study in which deleting IKKβ in hepatocytes accelerated proliferation. Page numbers were not supplied. (LLM, conf=0.86)
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Fausto N Campbell JS Riehle KJ 2006 Liver regeneration Hepatology 43 S45 53 16447274
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Kodama Y Taura K Miura K Schnabl B Osawa Y Brenner DA 2009 Anti-apoptotic effect of c-Jun N-terminal Kinase-1 through Mcl-1 stabilization in TNF-induced hepatocyte apoptosis Gastroenterology 136 1423 1434 19249395
Michalopoulos GK 2007 Liver regeneration J Cell Physiol 213 286 300 17559071 PMC2701258
Prusty BK Hedau S Singh A Kar P Das BC 2007 Selective suppression of NF-kB/p65 in hepatitis virus-infected pregnant women manifesting severe liver damage and high mortality Mol Med 13 518 526 17660862 PMC1933259

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Retracted

Mechanisms of crosstalk between TNF-induced NF-κB and JNK activation in hepatocytes
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Authors: Papa, S., Bubici, C., Zazzeroni, F., & Franzoso, G.
Affiliations: Imperial College London (GB)
University of L'Aquila (IT)
ORCID: Papa, Salvatore
Bubici, Concetta
Zazzeroni, Francesca
Franzoso, Guido
Venue: bchm
Publisher: Walter de Gruyter GmbH
Published: 2009-07-30
Volume: 390
Issue: 10
Pages: 965-976
ISSN: 1431-6730 (ISSN-L)
1437-4315
DOI: 10.1515/bc.2009.111
PMC: PMC2775491
OpenAlex: W110144856
Cited by: 156
References: 86
Citations by year: 2026: 9 · 2025: 9 · 2024: 8 · 2023: 9 · 2022: 11 · 2021: 12 · 2020: 10 · 2019: 6 · 2018: 9 · 2017: 11 · 2016: 7 · 2015: 9 · 2014: 7 · 2013: 13 · 2012: 9
FWCI: 1.04
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Locations: Biological Chemistry (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
Archivio Istituzionale della Ricerca - Università degli Studi dell Aquila (submittedVersion)
Spiral (Imperial College London) (submittedVersion)
Funders: Cancer Research UK (C26587-A8839)
National Cancer Institute (CA98583, CA84040, R01CA098583, R01CA084040)
Topics: Health Sciences › Medicine › Hepatology › Liver physiology and pathology
Life Sciences › Pharmacology, Toxicology and Pharmaceutics › Pharmacology › Drug-Induced Hepatotoxicity and Protection
Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
Keywords: NF-κB signaling, JNK signaling, TNF-α, hepatocyte death, liver injury, hepatotoxicity, c-Jun N-terminal kinase, caspases, interleukin-6, inflammatory cytokines, hepatocyte viability, hepatitis, hepatocellular carcinoma, signaling crosstalk
MeSH terms: Animals, Cell Physiological Phenomena, Hepatitis, Carcinoma, Hepatocellular, Humans, Liver Diseases, Signal Transduction, NF-kappa B, JNK Mitogen-Activated Protein Kinases

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

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