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Cited by 348Inflammasome and immune disordersLiver Disease Diagnosis and TreatmentLiver physiology and pathology

Role of inflammatory response in liver diseases: Therapeutic strategies

Open access
Campo, José A Del, Gallego, Paloma, Grande, Lourdes·2018·World Journal of Hepatology
DOI 10.4254/wjh.v10.i1.1PMC PMC5787673
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Abstract

Inflammation and tumorigenesis are tightly linked pathways impacting cancer development. Inflammasomes are key signalling platforms that detect pathogenic microorganisms, including hepatitis C virus (HCV) infection, and sterile stressors (oxidative stress, insulin resistance, lipotoxicity) able to activate pro-inflammatory cytokines interleukin-1β and IL-18. Most of the inflammasome complexes that have been described to date contain a NOD-like receptor sensor molecule. Redox state and autophagy can regulate inflammasome complex and, depending on the conditions, can be either pro- or anti-apoptotic. Acute and chronic liver diseases are cytokine-driven diseases as several proinflammatory cytokines (IL-1α, IL-1β, tumor necrosis factor-alpha, and IL-6) are critically involved in inflammation, steatosis, fibrosis, and cancer development. NLRP3 inflammasome gain of function aggravates liver disease, resulting in severe liver fibrosis and highlighting this pathway in the pathogenesis of non-alcoholic fatty liver disease. On the other hand, HCV infection is the primary catalyst for progressive liver disease and development of liver cancer. It is well established that HCV-induced IL-1β production by hepatic macrophages plays a critical and central process that promotes liver inflammation and disease. In this review, we aim to clarify the role of the inflammasome in the aggravation of liver disease, and how selective blockade of this main pathway may be a useful strategy to delay fibrosis progression in liver diseases.

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  • Inflammatory cytokines such as tumor necrosis factor or IL1B are common drivers of hepatocyte dedifferentiation and dysfunction.

    “inflammatory cytokines such as tumor necrosis factor or IL1B are well‐established common drivers of hepatocyte dedifferentiation and dysfunction (Del Campo et al, 2018; Hyun et al, 2020).”

    From An extended transcription factor regulatory network controls hepatocyte identity (2023) · cites this paper as Del Campo et al, 2018

    The section “Release of cytokines by immune cells” says cytokines including TNF-α and IL-1 can cause hepatocyte apoptosis, steatosis, and inflammation, supporting a role in hepatocyte injury and dysfunction. It does not say they drive hepatocyte dedifferentiation; the phenotypic transdifferentiation described in “Activation of HSCs and hepatic fibrosis” concerns hepatic stellate cells instead. Page numbers are unavailable in our copy. (LLM, conf=0.86)

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Authors
Campo, J. A. D., Gallego, P., & Grande, L.
Affiliations
Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (ES)
ORCID
Campo, José A Del
Venue
World Journal of Hepatology
Publisher
Baishideng Publishing Group Inc.
Published
2018-01-27
Volume
10
Issue
1
Pages
1-7
ISSN
1948-5182 (ISSN-L)
DOI
10.4254/wjh.v10.i1.1
PMC
PMC5787673
OpenAlex
W2784676168
Cited by
348
References
8
Citations by year
2026: 19 · 2025: 34 · 2024: 48 · 2023: 42 · 2022: 51 · 2021: 63 · 2020: 44 · 2019: 25 · 2018: 22
FWCI
3.78
Type
journal article
Language
en
Open access
Licence
cc-by-nc
Locations
  • World Journal of Hepatology (publishedVersion, cc-by-nc)
  • PubMed Central (publishedVersion, cc-by-nc)
  • PubMed (publishedVersion)
Funders
  • Servicio Andaluz de Salud
  • Instituto de Salud Carlos III (PI14/, PI14/01349)
  • European Regional Development Fund
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
  • Health Sciences › Medicine › Epidemiology › Liver Disease Diagnosis and Treatment
  • Health Sciences › Medicine › Hepatology › Liver physiology and pathology
Keywords
inflammasome, NLRP3 inflammasome, liver inflammation, liver fibrosis, non-alcoholic fatty liver disease, hepatitis C virus, IL-1β, IL-18, NOD-like receptors, hepatic macrophages, steatosis, carcinogenesis, autophagy, redox state, interleukin-6, TNF-α, treatment options

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