Evidence map›Paper›PMID 29924722›Full record

ReviewBiological chemistry2018

Interaction of volatile organic compounds and underlying liver disease: a new paradigm for risk.

Anna L Lang, Juliane I Beier

Abstract readReview
In one paragraph

Review in Biological chemistry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

38 citing papers in PubMed, 80 citations in OpenAlex.

  1. Article
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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 2 institutions in 1 country.

Anna L LangDepartment of Pharmacology and Toxicology, University of Louisville, Louisville, KY 40292, USA.
Juliane I BeierDepartment of Pharmacology and Toxicology, University of Louisville, Louisville, KY 40292, USA.
University of Louisville · USUniversity of Pittsburgh · US

Funding

Role of oxidized linoleic acid metabolites in the pathogenesis of alcoholic liver diseaseP20GM113226 · NIGMS · UNIVERSITY OF LOUISVILLE · PI HOOD, JOSHUA L. · 2016 to 2025
$24.1M
Superfund Training CoreP42ES023716 · NIEHS · UNIVERSITY OF LOUISVILLE · PI HEIN, DAVID W · 2017 to 2025
$18.1M
The Role of Nutrition in the Development/Progression of Alcohol-Induced Organ InjuryP50AA024337 · NIAAA · UNIVERSITY OF LOUISVILLE · PI CRAIG J. MCCLAIN · 2016 to 2026
$17.9M
Project 5 - Metabolomic Analysis of AtherothrombosisP20GM103492 · NIGMS · UNIVERSITY OF LOUISVILLE · PI HONG, KYUNG UK · 2012 to 2017
$13.8M
UOFL ENVIRONMENTAL HEALTH SCIENCES TRAINING PROGRAMT32ES011564 · NIEHS · UNIVERSITY OF LOUISVILLE · PI David W Hein, John Pierce Wise · 2004 to 2026
$7.1M
Enhancement of NAFLD risk by vinyl chloride: interaction of gut-liver-adipose axiK01DK096042 · NIDDK · UNIVERSITY OF LOUISVILLE · PI BEIER, JULIANE I · 2013 to 2017
$607k
Vinyl chloride-NAFLD interactionR03DK107912 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI BEIER, JULIANE I · 2016 to 2017
$155k
NIAAA NIH HHS P50 AA024337NIDDK NIH HHS K01 DK096042NIDDK NIH HHS R03 DK107912NIEHS NIH HHS P42 ES023716NIEHS NIH HHS T32 ES011564NIGMS NIH HHS P20 GM103492NIGMS NIH HHS P20 GM113226
6 · The paper itself

Abstract

Occupational and environmental exposures to industrial chemicals are known to cause hepatotoxicity and liver injury, in humans and in animal models. Historically, research has focused on severe acute liver injury (e.g. fulminant liver failure) or endstage diseases (e.g. cirrhosis and HCC). However, it has become recently recognized that toxicants can cause more subtle changes to the liver. For example, toxicant-associated steatohepatitis, characterized by hepatic steatosis, and inflammation, was recently recognized in an occupational cohort exposed to vinyl chloride. At high occupational levels, toxicants are sufficient to cause liver damage and disease even in healthy subjects with no comorbidities for liver injury. However, it is still largely unknown how exposure to toxicants initiate and possibly more importantly exacerbate liver disease, when combined with other factors, such as underlying non-alcoholic fatty liver disease caused by poor diet and/or obesity. With better understanding of the mechanism(s) and risk factors that mediate the initiation and progression of toxicant-induced liver disease, rational targeted therapy can be developed to better predict risk, as well as to treat or prevent this disease. The purpose of this review is to summarize established and proposed mechanisms of volatile organic compound-induced liver injury and to highlight key signaling events known or hypothesized to mediate these effects.

Indexed as

HumansLiverLiver DiseasesVolatile Organic CompoundsVolatile Organic Compoundsenvironmental liver diseasehepatotoxicitynon-alcoholic fatty liver disease (NAFLD)organochlorinestoxicanttoxicant-associated steatohepatitis (TASH)

Identifiers

PMID29924722
PMCPMC6181143
OpenAlexW2809059816

What Socratic holds

Textmetadata
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 Socratic graph.