Evidence map›Paper›PMID 29399273›Full record

ReviewWorld journal of hepatology2018

Role of inflammatory response in liver diseases: Therapeutic strategies.

José A Del Campo, Paloma Gallego, Lourdes Grande

Open access · diamondAbstract readReview
In one paragraph

Review in World journal of hepatology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 192 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
192citing papers in PubMed, 3 pooled it
24.6field-weighted citation impact, top 1% 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

192 citing papers in PubMed, 3 syntheses or guidelines pooled it, 341 citations in OpenAlex.

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  12. Physical exercise in liver diseases.Hepatology (Baltimore, Md.) · 2026
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132 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

3 authors at 2 institutions in 1 country.

José A Del CampoDepartment of Digestive Diseases, Valme University Hospital and CIBERehd, Sevilla 41014, Spain.
Paloma GallegoDepartment of Digestive Diseases, Valme University Hospital and CIBERehd, Sevilla 41014, Spain.
Lourdes GrandeDepartment of Digestive Diseases, Valme University Hospital and CIBERehd, Sevilla 41014, Spain.
Hospital Universitario de Valme · ESCentro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

Caspase-1FibrosisHepatitis C virusInflammasomeInterleukin-1αInterleukin-1βLiver diseaseNLRP3Non-alcoholic fatty liver diseaseTumor necrosis factor-alpha

Identifiers

PMID29399273
PMCPMC5787673
OpenAlexW2784676168

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.