Evidence map›Paper›PMID 29361514›Full record

ArticleDisease models & mechanisms2018

Inorganic arsenic causes fatty liver and interacts with ethanol to cause alcoholic liver disease in zebrafish.

Kathryn Bambino, Chi Zhang, Christine Austin, Chitra Amarasiriwardena, Manish Arora, Jaime Chu, Kirsten C Sadler

Open access · goldAbstract read
In one paragraph

Article in Disease models & mechanisms, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

22 citing papers in PubMed, 67 citations in OpenAlex.

  1. Article
  2. Article
  3. Mechanisms of Metal-Induced Hepatic Inflammation.Current environmental health reports · 2024
    Review
  4. Article
  5. Article
  6. Methods to Study Liver Disease Using Zebrafish Larvae.Methods in molecular biology (Clifton, N.J.) · 2024
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Mechanisms of Environmental Contributions to Fatty Liver Disease.Current environmental health reports · 2019
    Review
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

7 authors at 2 institutions in 2 countries.

Kathryn BambinoDepartment of Environmental Medicine and Public Health, Icahn School of Medicine at Mount Sinai, New York, New York 10029, USA.ORCID 0000-0001-8541-973X
Chi ZhangProgram in Biology, New York University Abu Dhabi, Saadiyat Island Campus, PO Box 129188 Abu Dhabi, United Arab Emirates.
Christine AustinDepartment of Environmental Medicine and Public Health, Icahn School of Medicine at Mount Sinai, New York, New York 10029, USA.
Chitra AmarasiriwardenaDepartment of Environmental Medicine and Public Health, Icahn School of Medicine at Mount Sinai, New York, New York 10029, USA.
Manish AroraDepartment of Environmental Medicine and Public Health, Icahn School of Medicine at Mount Sinai, New York, New York 10029, USA.
Jaime ChuDepartment of Pediatrics, Division of Pediatric Hepatology, Icahn School of Medicine at Mount Sinai, New York, New York 10029, USA.ORCID 0000-0002-9291-8630
Kirsten C SadlerProgram in Biology, New York University Abu Dhabi, Saadiyat Island Campus, PO Box 129188 Abu Dhabi, United Arab Emirates Kirsten.Edepli@nyu.edu.ORCID 0000-0002-1100-4125
Icahn School of Medicine at Mount Sinai · USNew York University Abu Dhabi · AE

Funding

The Mount Sinai Transdisciplinary Center on Early Environmental ExposuresP30ES023515 · NIEHS · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI Maria Jose Rosa · 2014 to 2026
$21.3M
Research Training Program in Pediatric ExposomicsT32HD049311 · NICHD · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI KECIA Nicole CARROLL, Robert O Wright · 2007 to 2026
$7.4M
Organic-metal mixtures and neurodevelopmentR01ES026033 · NIEHS · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI Manish Arora, Robert O Wright · 2016 to 2026
$6.1M
Understanding fatty liver disease using the zebrafish mutant, foie grasR01AA018886 · NIAAA · NEW YORK UNIVERSITY · PI SADLER EDEPLI, KIRSTEN C · 2009 to 2017
$2.4M
A novel role for p53 in congenital disorders of glycosylationK08DK101340 · NIDDK · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI CHU, JAIME C · 2013 to 2016
$554k
NIAAA NIH HHS R01 AA018886NICHD NIH HHS T32 HD049311NIDDK NIH HHS K08 DK101340NIEHS NIH HHS P30 ES023515NIEHS NIH HHS R01 ES026033
6 · The paper itself

Abstract

The rapid increase in fatty liver disease (FLD) incidence is attributed largely to genetic and lifestyle factors; however, environmental toxicants are a frequently overlooked factor that can modify the effects of more common causes of FLD. Chronic exposure to inorganic arsenic (iAs) is associated with liver disease in humans and animal models, but neither the mechanism of action nor the combinatorial interaction with other disease-causing factors has been fully investigated. Here, we examined the contribution of iAs to FLD using zebrafish and tested the interaction with ethanol to cause alcoholic liver disease (ALD). We report that zebrafish exposed to iAs throughout development developed specific phenotypes beginning at 4 days post-fertilization (dpf), including the development of FLD in over 50% of larvae by 5 dpf. Comparative transcriptomic analysis of livers from larvae exposed to either iAs or ethanol revealed the oxidative stress response and the unfolded protein response (UPR) caused by endoplasmic reticulum (ER) stress as common pathways in both these models of FLD, suggesting that they target similar cellular processes. This was confirmed by our finding that arsenic is synthetically lethal with both ethanol and a well-characterized ER-stress-inducing agent (tunicamycin), suggesting that these exposures work together through UPR activation to cause iAs toxicity. Most significantly, combined exposure to sub-toxic concentrations of iAs and ethanol potentiated the expression of UPR-associated genes, cooperated to induce FLD, reduced the expression of

Indexed as

AnimalsArsenicDisease SusceptibilityEmbryo, NonmammalianEndoplasmic Reticulum StressEthanolFatty LiverLarvaLiverLiver Diseases, AlcoholicModels, BiologicalOxidative StressSignal TransductionZebrafishArsenicEthanolArsenicEnvironmental exposureEthanolFatty liver disease

Identifiers

PMID29361514
PMCPMC5894941
OpenAlexW2777559376

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.