Evidence map›Paper›PMID 30560047›Full record

ArticleCurrent pharmacology reports2018

Mechanisms of Inflammatory Liver Injury and Drug-Induced Hepatotoxicity.

Benjamin L Woolbright, Hartmut Jaeschke

Open access · greenAbstract read
In one paragraph

Article in Current pharmacology reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
9.3field-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

46 citing papers in PubMed, 98 citations in OpenAlex.

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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

2 authors at 1 institution in 1 country.

Benjamin L WoolbrightDepartment of Urology, University of Kansas Medical Center, Kansas City, KS, USA.
Hartmut JaeschkePharmacology, Toxicology & Therapeutics, University of Kansas Medical Center, Kansas City, KS, USA.
University of Kansas Medical Center · US

Funding

Nuclear Receptors in Liver Health and DiseaseP20GM103549 · NIGMS · UNIVERSITY OF KANSAS MEDICAL CENTER · PI JAESCHKE, HARTMUT W. · 2012 to 2015
$8.1M
Pilot Grants ProgramP30GM118247 · NIGMS · UNIVERSITY OF KANSAS MEDICAL CENTER · PI JAESCHKE, HARTMUT W. · 2016 to 2020
$5.5M
NEUTROPHIL-INDUCED LIVER INJURY TOXICITYR01AA012916 · NIAAA · UNIVERSITY OF KANSAS MEDICAL CENTER · PI JAESCHKE, HARTMUT W. · 2001 to 2012
$2.9M
Autophagy and Drug-Induced Liver InjuryR01DK102142 · NIDDK · UNIVERSITY OF KANSAS MEDICAL CENTER · PI DING, WEN-XING, JAESCHKE, HARTMUT W. · 2014 to 2022
$2.7M
NIAAA NIH HHS R01 AA012916NIDDK NIH HHS R01 DK102142NIGMS NIH HHS P20 GM103549NIGMS NIH HHS P30 GM118247
6 · The paper itself

Abstract

purpose of reviewThis article provides a brief overview of mechanisms of inflammatory liver injury and how this applies to drug hepatotoxicity with a particular emphasis on the role of inflammation in acetaminophen-induced liver injury. RECENT

findingsSignificant progress has been made in the last decade in our understanding of the initiation of sterile inflammation after necrotic cell death by the release of damage-associated molecular patterns and their recognition by toll-like receptors and others on macrophages. These events trigger the formation of cytokines and chemokines directly or with assistance of inflammasome activation thereby activating and recruiting leukocytes including neutrophils and monocyte-derived macrophages into the necrotic areas. Although this sterile inflammatory response is mainly geared towards the removal of necrotic cell debris and preparation of regeneration, there are conditions where these innate immune cells can aggravate the initial injury. The mechanisms and controversial findings of the innate immunity are being discussed in detail. In contrast, drug metabolism and formation of a reactive metabolite that binds to proteins in the absence of extensive cell death, can induce an adaptive immune response, which eventually also results in severe liver injury. However, the initiating event appears to be the formation of protein adducts, which act as haptens to activate an adaptive immune response. Overall, these mechanisms are less well understood. SUMMARY: The past decade has revolutionized our understanding of the mechanisms that control the interplay between cell death and innate or adaptive immune responses. This report provides an update on these mechanisms.

Indexed as

acetaminophenadaptive immunitydrug-induced liver injuryinnate immunitymonocytesneutrophilsreactive metabolites

Identifiers

PMID30560047
PMCPMC6294466
OpenAlexW2811069251

What OpenQuestion holds

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LicenceTDM
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.