Evidence map›Paper›PMID 21633650›Full record

ReviewWorld journal of gastroenterology2011

Epigenetic regulation in alcoholic liver disease.

Pranoti Mandrekar

Open access · hybridAbstract readReview
In one paragraph

Review in World journal of gastroenterology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
6.5field-weighted citation impact, top 3% 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

52 citing papers in PubMed, 91 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Review
  5. Global DNA methylation patterns in Alcohol Use Disorder.Genetics and molecular biology · 2024
    Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. Alcohol-Related Liver Disease: Basic Mechanisms and Clinical Perspectives.International journal of molecular sciences · 2021
    Review
  11. Review
  12. Review
  13. Article
  14. Targeting Epigenetic Mechanisms to Alleviate Alcoholic Steatosis.Cellular and molecular gastroenterology and hepatology · 2020
    Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Alcoholic liver disease.Nature reviews. Disease primers · 2018
    Review
  20. Emerging Role of Epigenetic Mechanisms in Alcohol Addiction.Alcoholism, clinical and experimental research · 2017
    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

1 author at 1 institution in 1 country.

Pranoti MandrekarDepartment of Medicine, University of Massachusetts Medical School, 364 Plantation Street, Worcester, MA 01605, United States. pranoti.mandrekar@umassmed.edu
University of Massachusetts Chan Medical School · US

Funding

Role of heat shock protein 90 in alcoholic liver diseaseR01AA017986 · NIAAA · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI Pranoti Mandrekar · 2009 to 2026
$6.7M
Regulation of MCP-1 and chemokine receptor 2 (CCR2) in alcoholic liver diseaseR21AA017545 · NIAAA · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI MANDREKAR, PRANOTI · 2010 to 2010
$247k
NIAAA NIH HHS AA017545NIAAA NIH HHS AA017986NIAAA NIH HHS R01 AA017986NIAAA NIH HHS R21 AA017545
6 · The paper itself

Abstract

Alcoholic liver disease (ALD) is characterized by steatosis or fat deposition in the liver and inflammation, which leads to cirrhosis and hepatocellular carcinoma. Induction of target genes without involving changes in DNA sequence seems to contribute greatly to liver injury. Chromatin modifications including alterations in histones and DNA, as well as post-transcriptional changes collectively referred to as epigenetic effects are altered by alcohol. Recent studies have pointed to a significant role for epigenetic mechanisms at the nucleosomal level influencing gene expression and disease outcome in ALD. Specifically, epigenetic alterations by alcohol include histone modifications such as changes in acetylation and phosphorylation, hypomethylation of DNA, and alterations in miRNAs. These modifications can be induced by alcohol-induced oxidative stress that results in altered recruitment of transcriptional machinery and abnormal gene expression. Delineating these mechanisms in initiation and progression of ALD is becoming a major area of interest. This review summarizes key epigenetic mechanisms that are dysregulated by alcohol in the liver. Alterations by alcohol in histone and DNA modifications, enzymes related to histone acetylation such as histone acetyltransferases, histone deacetylases and sirtuins, and methylation enzymes such as DNA methyltransferases are discussed. Chromatin modifications and miRNA alterations that result in immune cell dysfunction contributing to inflammatory cytokine production in ALD is reviewed. Finally, the role of alcohol-mediated oxidative stress in epigenetic regulation in ALD is described. A better understanding of these mechanisms is crucial for designing novel epigenetic based therapies to ameliorate ALD.

Indexed as

Epigenesis, GeneticEthanolGene ExpressionHumansLiverLiver Diseases, AlcoholicOxidative StressEthanolAcetylationAlcoholDNA methylationEpigeneticsGenesHistonesmiRNA

Identifiers

PMID21633650
PMCPMC3103803
OpenAlexW2163978132

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.