Evidence map›Paper›PMID 38908436›Full record

ReviewJournal of hepatology2024

Inflammasomes in chronic liver disease: Hepatic injury, fibrosis progression and systemic inflammation.

Vlad Taru, Gyongyi Szabo, Wajahat Mehal, Thomas Reiberger

Abstract readReview
In one paragraph

Review in Journal of hepatology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 175 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
175citing papers in PubMed, 5 pooled it
–field-weighted citation impact
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

175 citing papers in PubMed, 5 syntheses or guidelines pooled it.

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  6. Review
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  8. Actin cytoskeletal dynamics in hepatic myofibroblasts and fibrosis.Nature reviews. Gastroenterology & hepatology · 2026
    Review
  9. E3 Ubiquitin Ligases in MASH-Associated Liver Fibrosis: Mechanisms and Therapeutic Opportunities.Liver international : official journal of the International Association for the Study of the Liver · 2026
    Review
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115 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.

Vlad TaruDivision of Gastroenterology and Hepatology, Department of Medicine III, Medical University of Vienna, Vienna, Austria; Christian-Doppler Laboratory for Portal Hypertension and Liver Fibrosis, Medical University of Vienna, Vienna, Austria; Iuliu Hatieganu University of Medicine and Pharmacy, 4(th) Dept. of Internal Medicine, Cluj-Napoca, Romania.
Gyongyi SzaboDepartment of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, USA.
Wajahat MehalSection of Digestive Diseases, Yale School of Medicine, New Haven, CT, USA; West Haven Veterans Medical Center, West Haven, CT, USA. Electronic address: wajahat.mehal@yale.edu.
Thomas ReibergerDivision of Gastroenterology and Hepatology, Department of Medicine III, Medical University of Vienna, Vienna, Austria; Christian-Doppler Laboratory for Portal Hypertension and Liver Fibrosis, Medical University of Vienna, Vienna, Austria; Center for Molecular Medicine (CeMM) of the Austrian Academy of Science, Vienna, Austria.

Funding

TLR4 Signaling in alcoholic liver diseaseR01AA017729 · NIAAA · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI SZABO, GYONGYI · 2009 to 2021
$4.3M
Alcoholic Hepatitis Clinical and Translational Network Late Phase Clinical Trials and Observational Studies 4/9U01AA026977 · NIAAA · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI SZABO, GYONGYI · 2018 to 2022
$1.8M
BLRD VA I01 BX003259NIAAA NIH HHS R01 AA017729NIAAA NIH HHS U01 AA026977
6 · The paper itself

Abstract

Chronic liver disease leads to hepatocellular injury that triggers a pro-inflammatory state in several parenchymal and non-parenchymal hepatic cell types, ultimately resulting in liver fibrosis, cirrhosis, portal hypertension and liver failure. Thus, an improved understanding of inflammasomes - as key molecular drivers of liver injury - may result in the development of novel diagnostic or prognostic biomarkers and effective therapeutics. In liver disease, innate immune cells respond to hepatic insults by activating cell-intrinsic inflammasomes via toll-like receptors and NF-κB, and by releasing pro-inflammatory cytokines (such as IL-1β, IL-18, TNF-α and IL-6). Subsequently, cells of the adaptive immune system are recruited to fuel hepatic inflammation and hepatic parenchymal cells may undergo gasdermin D-mediated programmed cell death, termed pyroptosis. With liver disease progression, there is a shift towards a type 2 inflammatory response, which promotes tissue repair but also fibrogenesis. Inflammasome activation may also occur at extrahepatic sites, such as the white adipose tissue in MASH (metabolic dysfunction-associated steatohepatitis). In end-stage liver disease, flares of inflammation (e.g., in severe alcohol-related hepatitis) that spark on a dysfunctional immune system, contribute to inflammasome-mediated liver injury and potentially result in organ dysfunction/failure, as seen in ACLF (acute-on-chronic liver failure). This review provides an overview of current concepts regarding inflammasome activation in liver disease progression, with a focus on related biomarkers and therapeutic approaches that are being developed for patients with liver disease.

Indexed as

Disease ProgressionInflammasomesInflammationLiver CirrhosisAnimalsChronic DiseaseHumansLiverLiver DiseasesInflammasomesalcohol-related liver diseasecirrhosishepatic stellate cellinflammasomeKupffer cellliver fibrosismacrophagemetabolic dysfunction-associated steatotic liver diseasetoll-like receptor, nod-like receptor

Identifiers

PMID38908436
PMCPMC11881887

What OpenQuestion holds

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LicenceCC BY
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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.