Evidence map›Paper›PMID 32582865›Full record

ArticleHepatoma research2020

The mechanism of dysbiosis in alcoholic liver disease leading to liver cancer.

Nahum Méndez-Sánchez, Alejandro Valencia-Rodriguez, Alfonso Vera-Barajas, Ludovico Abenavoli, Emidio Scarpellini, Guadalupe Ponciano-Rodriguez, David Q-H Wang

Open access · diamondAbstract read
In one paragraph

Article in Hepatoma research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
4.5field-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

24 citing papers in PubMed, 44 citations in OpenAlex.

  1. Review
  2. Review
  3. Circulating urobilinogen augments inflammation and corticosteroid non-response in severe alcohol-induced hepatitis.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Article
  4. The oncobiome; what, so what, now what?Microbiome research reports · 2025
    Review
  5. Review
  6. Article
  7. Transcription factorBiomolecules & biomedicine · 2024
    Article
  8. The Impact of ProbioticLife (Basel, Switzerland) · 2024
    Review
  9. Clinical Significance of Serum Bile Acid Profiles in Fatty Liver.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024
    Article
  10. Article
  11. Review
  12. Review
  13. Review
  14. Review
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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

7 authors at 2 institutions in 1 country.

Nahum Méndez-SánchezLiver Research Unit, Medica Sur Clinic & Foundation, Mexico City 14050, Mexico.
Alejandro Valencia-RodriguezLiver Research Unit, Medica Sur Clinic & Foundation, Mexico City 14050, Mexico.
Alfonso Vera-BarajasLiver Research Unit, Medica Sur Clinic & Foundation, Mexico City 14050, Mexico.
Ludovico AbenavoliDepartment of Health Sciences, University "Magna Graecia" Viale Europa, Catanzaro 88100, Italy.
Emidio ScarpelliniClinical Nutrition Unit, and Internal Medicine Unit, "Madonna del Soccorso" General Hospital, Via Luciano Manara 7, San Benedetto del Tronto (AP) 63074, Italy.
Guadalupe Ponciano-RodriguezPublic Health Department, Faculty of Medicine, National Autonomous University of Mexico, Mexico City 04510, Mexico.
David Q-H WangDepartment of Medicine and Genetics, Division of Gastroenterology and Liver Diseases, Marion Bessin Liver Research Center, Einstein-Mount Sinai Diabetes Research Center, Albert Einstein College of Medicine, Bronx, NY 10461, USA.
Hospital Médica Sur · MXUniversidad Nacional Autónoma de México · MX

Funding

GPR30 and hepatic cholesterol metabolismR01DK126369 · NIDDK · ALBERT EINSTEIN COLLEGE OF MEDICINE · PI PESSIN, JEFFREY E. · 2020 to 2023
$1.9M
Apolipoprotein A5 and Gallstone FormationR01DK114516 · NIDDK · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI WANG, DAVID Q · 2018 to 2021
$1.5M
GPR30 and Hepatic Cholesterol HomeostasisR01DK106249 · NIDDK · SAINT LOUIS UNIVERSITY · PI WANG, DAVID Q · 2015 to 2017
$1.0M
Gene therapy of alcoholic liver diseaseR21AA025737 · NIAAA · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI WANG, DAVID Q · 2017 to 2018
$438k
NIAAA NIH HHS R21 AA025737NIDDK NIH HHS R01 DK106249NIDDK NIH HHS R01 DK114516NIDDK NIH HHS R01 DK126369
6 · The paper itself

Abstract

Currently, alcoholic liver disease (ALD) is one of the most prevalent chronic liver diseases worldwide, representing one of the main etiologies of cirrhosis and hepatocellular carcinoma (HCC). Although we do not know the exact mechanisms by which only a selected group of patients with ALD progress to the final stage of HCC, the role of the gut microbiota within the progression to HCC has been intensively studied in recent years. To date, we know that alcohol-induced gut dysbiosis is an important feature of ALD with important repercussions on the severity of this disease. In essence, an increased metabolism of ethanol in the gut induced by an excessive alcohol consumption promotes gut dysfunction and bacterial overgrowth, setting a leaky gut. This causes the translocation of bacteria, endotoxins, and ethanol metabolites across the enterohepatic circulation reaching the liver, where the recognition of the pathogen-associated molecular patterns via specific Toll-like receptors of liver cells will induce the activation of the nuclear factor kappa-B pathway, which releases pro-inflammatory cytokines and chemokines. In addition, the mitogenic activity of hepatocytes will be promoted and cellular apoptosis will be inhibited, resulting in the development of HCC. In this context, it is not surprising that microbiota-regulating drugs have proven effectiveness in prolonging the overall survival of patients with HCC, making attractive the implementation of these drugs as co-adjuvant for HCC treatment.

Indexed as

Alcoholic liver diseasedysbiosisgut microbiotahepatocellular carcinoma

Identifiers

PMID32582865
PMCPMC7313221
OpenAlexW3008870263

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.