Evidence map›Paper›PMID 19291818›Full record

ReviewWorld journal of gastroenterology2009

Is the iron regulatory hormone hepcidin a risk factor for alcoholic liver disease?

Duygu Dee Harrison-Findik

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in World journal of gastroenterology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

26 citing papers in PubMed, 53 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Liver Iron Loading in Alcohol-Associated Liver Disease.The American journal of pathology · 2023
    Review
  6. Article
  7. Article
  8. Review
  9. Effects of Lactobacillus casei on Iron Metabolism and Intestinal Microflora in Rats Exposed to Alcohol and Iron.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2022
    Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Monitoring trace elements generated by automobiles: air pollutants with possible health impacts.Environmental science and pollution research international · 2013
    Article
  20. Article
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

1 author at 1 institution in 1 country.

Duygu Dee Harrison-FindikDivision of Gastroenterology and Hepatology, Department of Internal Medicine, University of Nebraska Medical Center, Omaha, NE, 68198-5820, United States. dharrisonfindik@unmc.edu
Nebraska Medical Center · US

Funding

THE REDOX-MEDIATED REGULATION OF IRON-RESPONSIVE GENE EXPRESSION IN LIVERP20RR017675 · NCRR · UNIVERSITY OF NEBRASKA LINCOLN · PI GRASS, GREGOR · 2002 to 2011
$20.4M
Role of Mitochondria in the Regulation of Iron metabolism by AlcoholR01AA017738 · NIAAA · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI HARRISON-FINDIK, DUYGU DEE DEE · 2008 to 2012
$1.6M
NCRR NIH HHS 2P20RR017675NCRR NIH HHS P20 RR017675NIAAA NIH HHS R01 AA017738NIAAA NIH HHS R01AA017738-01
6 · The paper itself

Abstract

Despite heavy consumption over a long period of time, only a small number of alcoholics develop alcoholic liver disease. This alludes to the possibility that other factors, besides alcohol, may be involved in the progression of the disease. Over the years, many such factors have indeed been identified, including iron. Despite being crucial for various important biological processes, iron can also be harmful due to its ability to catalyze Fenton chemistry. Alcohol and iron have been shown to interact synergistically to cause liver injury. Iron-mediated cell signaling has been reported to be involved in the pathogenesis of experimental alcoholic liver disease. Hepcidin is an iron-regulatory hormone synthesized by the liver, which plays a pivotal role in iron homeostasis. Both acute and chronic alcohol exposure suppress hepcidin expression in the liver. The sera of patients with alcoholic liver disease, particularly those exhibiting higher serum iron indices, have also been reported to display reduced prohepcidin levels. Alcohol-mediated oxidative stress is involved in the inhibition of hepcidin promoter activity and transcription in the liver. This in turn leads to an increase in intestinal iron transport and liver iron storage. Hepcidin is expressed primarily in hepatocytes. It is noteworthy that both hepatocytes and Kupffer cells are involved in the progression of alcoholic liver disease. However, the activation of Kupffer cells and TNF-alpha signaling has been reported not to be involved in the down-regulation of hepcidin expression by alcohol in the liver. Alcohol acts within the parenchymal cells of the liver to suppress the synthesis of hepcidin. Due to its crucial role in the regulation of body iron stores, hepcidin may act as a secondary risk factor in the progression of alcoholic liver disease. The clarification of the mechanisms by which alcohol disrupts iron homeostasis will allow for further understanding of the pathogenesis of alcoholic liver disease.

Indexed as

Antimicrobial Cationic PeptidesDown-RegulationEthanolHepcidinsHomeostasisIronKupffer CellsLiver Diseases, AlcoholicPromoter Regions, GeneticRisk FactorsTranscription, GeneticAntimicrobial Cationic PeptidesEthanolHepcidinsIron

Identifiers

PMID19291818
PMCPMC2658862
OpenAlexW2099217986

What OpenQuestion holds

Textmetadata
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.