Evidence map›Paper›PMID 39735421›Full record

ArticleeGastroenterology2024

Cell-to-cell and organ-to-organ crosstalk in the pathogenesis of alcohol-associated liver disease.

Hui Gao, Yanchao Jiang, Ge Zeng, Nazmul Huda, Themis Thoudam, Zhihong Yang, Suthat Liangpunsakul, Jing Ma

Abstract read
In one paragraph

Article in eGastroenterology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
–field-weighted citation impact
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

54 citing papers in PubMed.

  1. Article
  2. Review
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  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. The Link between Alcohol Consumption and Kidney Injury.The American journal of pathology · 2026
    Review
  14. Review
  15. Cholestasis in Alcohol-Associated Liver Disease.The American journal of pathology · 2026
    Review
  16. Article
  17. Article
  18. Review
  19. 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

8 authors.

Hui GaoDepartment of Medicine, Indiana University School of Medicine, Indianapolis, Indiana, USA.
Yanchao JiangDepartment of Medicine, Indiana University School of Medicine, Indianapolis, Indiana, USA.
Ge ZengDepartment of Medicine, Indiana University School of Medicine, Indianapolis, Indiana, USA.
Nazmul HudaDepartment of Medicine, Indiana University School of Medicine, Indianapolis, Indiana, USA.
Themis ThoudamDepartment of Medicine, Indiana University School of Medicine, Indianapolis, Indiana, USA.
Zhihong YangDepartment of Medicine, Indiana University School of Medicine, Indianapolis, Indiana, USA.
Suthat LiangpunsakulDepartment of Medicine, Indiana University School of Medicine, Indianapolis, Indiana, USA.
Jing MaDepartment of Medicine, Indiana University School of Medicine, Indianapolis, Indiana, USA.ORCID 0000-0002-2671-3792

Funding

Indiana Clinical and Translational Sciences InstituteUM1TR004402 · NCATS · INDIANA UNIVERSITY INDIANAPOLIS · PI Sharon M Moe, Sarah Elizabeth Wiehe · 2023 to 2026
$21.6M
FKBP5 in the pathogenesis of alcohol-associated liver diseaseR01AA030312 · NIAAA · INDIANA UNIVERSITY INDIANAPOLIS · PI Suthat Liangpunsakul · 2022 to 2026
$1.8M
Long Noncoding RNA H19 Mediating Alternative Splicing in ALD PathogenesisR01AA030993 · NIAAA · INDIANA UNIVERSITY INDIANAPOLIS · PI Zhihong Yang · 2023 to 2026
$1.6M
Immunological Profiles and prognostic outcomes in patients with alcoholic hepatitisU01AA026917 · NIAAA · INDIANA UNIVERSITY INDIANAPOLIS · PI LIANGPUNSAKUL, SUTHAT · 2018 to 2022
$1.2M
Novel animal models to study miRNA-mediated alcoholic liver diseaseUH3AA026903 · NIAAA · INDIANA UNIVERSITY INDIANAPOLIS · PI LIANGPUNSAKUL, SUTHAT · 2020 to 2022
$1.2M
Integrating LncRNA to Methionine Metabolism in Alcoholic Fatty LiverK01AA026385 · NIAAA · INDIANA UNIVERSITY INDIANAPOLIS · PI YANG, ZHIHONG · 2018 to 2022
$807k
Novel animal models to study miRNA-mediated alcoholic liver diseaseUH2AA026903 · NIAAA · INDIANA UNIVERSITY INDIANAPOLIS · PI LIANGPUNSAKUL, SUTHAT · 2018 to 2019
$447k
Mechanism of neutrophilic NCF1 in alcohol-associated liver disease pathogenesisK99AA031067 · NIAAA · INDIANA UNIVERSITY INDIANAPOLIS · PI MA, JING · 2023 to 2024
$294k
Mechanism of PDK4 and MAM axis in alcohol-associated liver diseaseI01BX006202 · VA · RLR VA MEDICAL CENTER · PI Suthat Liangpunsakul · 2024 to 2026
–
Serum Proteomic Profiles as Biomarkers of Abusive Alcohol ConsumptionI01CX000361 · VA · RLR VA MEDICAL CENTER · PI LIANGPUNSAKUL, SUTHAT · 2012 to 2025
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BLRD VA I01 BX006202CSRD VA I01 CX000361NCATS NIH HHS UM1 TR004402NIAAA NIH HHS K01 AA026385NIAAA NIH HHS K99 AA031067NIAAA NIH HHS R01 AA030312NIAAA NIH HHS R01 AA030993NIAAA NIH HHS U01 AA026917NIAAA NIH HHS UH2 AA026903
6 · The paper itself

Abstract

Alcohol-associated liver disease (ALD) is a growing global health concern and its prevalence and severity are increasing steadily. While bacterial endotoxin translocation into the portal circulation is a well-established key factor, recent evidence highlights the critical role of sterile inflammation, triggered by diverse stimuli, in alcohol-induced liver injury. This review provides a comprehensive analysis of the complex interactions within the hepatic microenvironment in ALD. It examines the contributions of both parenchymal cells, like hepatocytes, and non-parenchymal cells, such as hepatic stellate cells, Kupffer cells, neutrophils, and liver sinusoidal endothelial cells, in driving the progression of the disease. Additionally, we explored the involvement of key mediators, including cytokines, chemokines and inflammasomes, which regulate inflammatory responses and promote liver injury and fibrosis. A particular focus has been placed on extracellular vesicles (EVs) as essential mediators of intercellular communication both within and beyond the liver. These vesicles facilitate the transfer of signalling molecules, such as microRNAs and proteins, which modulate immune responses, fibrogenesis and lipid metabolism, thereby influencing disease progression. Moreover, we underscore the importance of organ-to-organ crosstalk, particularly in the gut-liver axis, where dysbiosis and increased intestinal permeability lead to microbial translocation, exacerbating hepatic inflammation. The adipose-liver axis is also highlighted, particularly the impact of adipokines and free fatty acids from adipose tissue on hepatic steatosis and inflammation in the context of alcohol consumption.

Identifiers

PMID39735421
PMCPMC11674000

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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.