NF-κB in the liver—linking injury, fibrosis and hepatocellular carcinoma

Luedde, Tom; Schwabe, Robert F.

doi:10.1038/nrgastro.2010.213

Cited by 1,345Liver physiology and pathologyNF-κB Signaling PathwaysHepatocellular Carcinoma Treatment and Prognosis

NF-κB in the liver—linking injury, fibrosis and hepatocellular carcinoma

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Luedde, Tom, Schwabe, Robert F.·2011·Nature Reviews Gastroenterology & Hepatology

DOI 10.1038/nrgastro.2010.213PMC PMC3295539

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Abstract

Hepatic cirrhosis and hepatocellular carcinoma (HCC) are the most common causes of death in patients with chronic liver disease. Chronic liver injury of virtually any etiology triggers inflammatory and wound-healing responses that in the long run promote the development of hepatic fibrosis and HCC. Here, we review the role of the transcription factor nuclear factor-κB (NF-κB), a master regulator of inflammation and cell death, in the development of hepatocellular injury, liver fibrosis and HCC, with a particular focus on the role of NF-κB in different cellular compartments of the liver. We propose that NF-κB acts as a central link between hepatic injury, fibrosis and HCC, and that it may represent a target for the prevention or treatment of liver fibrosis and HCC. However, NF-κB acts as a two-edged sword and inhibition of NF-κB may not only exert beneficial effects but also negatively impact hepatocyte viability, especially when NF-κB inhibition is pronounced. Finding appropriate targets or identifying drugs that either exert only a moderate effect on NF-κB activity or that can be specifically delivered to nonparenchymal cells will be essential to avoid the increase in liver injury associated with complete NF-κB blockade in hepatocytes.

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NF-κB activation additionally causes significantly increased resistance against apoptosis in activated hepatic stellate cells.
“However, the decisive factor is that NF-κB-activation additionally causes a significantly increased resistance against apoptosis in aHSCs.[21]”
From Nuclear receptors in liver fibrosis (2021) · cites this paper as [21]

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Inhibition of NFκB in activated rat hepatic stellate cells by proteasome inhibitors and an IκB super-repressor
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Induction of Hepatitis by JNK-Mediated Expression of TNF-α
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The chemokine CCL21 modulates lymphocyte recruitment and fibrosis in chronic hepatitis C1 1The authors thank Wanda Delogu and Nadia Navari for skillful technical help, Dr. Roberto G. Romanelli for help in collecting liver biopsy specimens, and Dr. Mario Strazzabosco (Ospedali Riuniti di Bergamo, Italy) for providing part of the tissue samples with primary biliary cirrhosis.
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Activation of NF-kappaB, AP-1 and STAT transcription factors is a frequent and early event in human hepatocellular carcinomas
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Role of TLR9 in hepatic stellate cells and experimental liver fibrosis
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Angiotensin II Activates IκB Kinase Phosphorylation of RelA at Ser536 to Promote Myofibroblast Survival and Liver Fibrosis
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THE ROLE OF INTESTINAL BACTERIA IN THE DEVELOPMENT OF DIETARY CIRRHOSIS IN RATS
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Hepatic NF-κB essential modulator deficiency prevents obesity-induced insulin resistance but synergizes with high-fat feeding in tumorigenesis
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Reversibility of Cirrhosis in Patients Cured of Thalassemia by Bone Marrow Transplantation
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Liver NF‐κB and AP‐1 DNA Binding in Obese Patients
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Constitutively active NF-κB triggers systemic TNFα-dependent inflammation and localized TNFα-independent inflammatory diseasePreprint
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Normal epidermal differentiation but impaired skin-barrier formation upon keratinocyte-restricted IKK1 ablation
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IKK1 and IKK2 cooperate to maintain bile duct integrity in the liver
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Signaling Pathways in Liver Diseases
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Inhibitor of nuclear factor kappaB kinase deficiency enhances oxidative stress and prolongs c-Jun NH2-terminal kinase activation induced by arsenic.
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the C-Rel Subunit of Nuclear Factor-κB Regulates Murine Liver Inflammation, Wound-Healing, and Hepatocyte Proliferation
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Nuclear factor-κB in the liver of patients with chronic hepatitis C: Decreased RelA expression is associated with enhanced fibrosis progression
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Increased Expression of iASPP, Regulated by Hepatitis B Virus X Protein-Mediated NF-κB Activation, in Hepatocellular Carcinoma
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Bile acid-microbiota crosstalk in gastrointestinal inflammation and carcinogenesis
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Endoplasmic reticulum stress signalling and the pathogenesis of non-alcoholic fatty liver disease.
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Role of the Microenvironment in the Pathogenesis and Treatment of Hepatocellular Carcinoma
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Pharmacological Inhibition of the Chemokine CCL2 (MCP-1) Diminishes Liver Macrophage Infiltration and Steatohepatitis in Chronic Hepatic Injury
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Inflammation-induced IgA+ cells dismantle anti-liver cancer immunity
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Cancer-Associated Fibroblasts Regulate Tumor-Initiating Cell Plasticity in Hepatocellular Carcinoma through c-Met/FRA1/HEY1 Signaling
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Obesity-Induced TNFα and IL-6 Signaling: The Missing Link between Obesity and Inflammation—Driven Liver and Colorectal Cancers
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Curcumin effectively inhibits oncogenic NF-κB signaling and restrains stemness features in liver cancer
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Authors: Luedde, T., & Schwabe, R. F.
Affiliations: Universitätsklinikum Aachen (DE)
Columbia University Irving Medical Center (US)
Corresponding author: Luedde, Tom
Schwabe, Robert F.
ORCID: Luedde, Tom
Schwabe, Robert F.
Venue: Nature Reviews Gastroenterology & Hepatology
Publisher: Springer Science and Business Media LLC
Published: 2011-02
Volume: 8
Issue: 2
Pages: 108-118
ISSN: 1759-5045 (ISSN-L)
1759-5053
DOI: 10.1038/nrgastro.2010.213
PMC: PMC3295539
OpenAlex: W1976777085
Cited by: 1,345
References: 137
Citations by year: 2026: 97 · 2025: 99 · 2024: 119 · 2023: 109 · 2022: 122 · 2021: 156 · 2020: 120 · 2019: 95 · 2018: 79 · 2017: 76 · 2016: 66 · 2015: 68 · 2014: 51 · 2013: 38 · 2012: 42
FWCI: 5.65
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: www.springer.com/tdm (tdm)
Locations: Nature Reviews Gastroenterology & Hepatology (publishedVersion)
PubMed (publishedVersion)
Europe PMC (PubMed Central) (acceptedVersion)
PubMed Central (acceptedVersion)
Funders: National Institutes of Health (5u54ca126513-03)
National Institute on Alcohol Abuse and Alcoholism (R01AA020211)
National Cancer Institute (U54 CA126513.)
National Institute of Diabetes and Digestive and Kidney Diseases (R01DK076920)
National Center for Complementary and Integrative Health (R21AT003878)
Topics: Health Sciences › Medicine › Hepatology › Liver physiology and pathology
Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
Health Sciences › Medicine › Hepatology › Hepatocellular Carcinoma Treatment and Prognosis
Keywords: NF-κB, liver fibrosis, hepatocellular carcinoma, chronic liver disease, liver cirrhosis, chronic liver injury, liver inflammation, hepatocytes, non-parenchymal liver cells, NF-κB inhibition, hepatocyte viability
MeSH terms: Cell Survival, Fibrosis, Carcinoma, Hepatocellular, Homeostasis, Humans, Liver, Liver Neoplasms, NF-kappa B, Hepatocytes

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NF-κB in the liver—linking injury, fibrosis and hepatocellular carcinoma

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