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Cited by 5Liver physiology and pathologyAlcohol Consumption and Health EffectsLiver Disease Diagnosis and Treatment

Continuous Activation of C/EBPβ Transcription Factor Prevents Fibrosis Resolution After Alcohol Cessation

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Schonfeld, Michael, Nataraj, Kruti, Mah, Samson, Weinman, Steven, Tikhanovich, Irina·2025·Cellular and Molecular Gastroenterology and Hepatology
DOI 10.1016/j.jcmgh.2025.101525PMC PMC12206133
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Abstract

BACKGROUND & AIMS: Abstinence is an important therapeutic intervention for patients with alcohol-associated liver disease (ALD). However, fibrosis improvement after cessation is not uniform and some patients do not improve. METHODS: Mice were fed high-fat diet with 20% alcohol in the drinking water for 20 weeks (ALD) followed by 4 weeks of chow diet with plain water (resolution). scATAC-seq dataset was analyzed using Signac R package. Cebpb floxed mice received AAV-TBG-Cre or AAV-control at the time of alcohol cessation. Hepatocyte-macrophage and endothelial cell-hepatocytes crosstalk was investigated using a Transwell coculture system. To test the role of angiopoietin mice were treated with recombinant angiopoietin-1, 1 week after alcohol cessation. RESULTS: We analyzed differentially accessible regions in hepatocytes from control, ALD, or 4 weeks post alcohol cessation mice and identified transcription factors activated in ALD that remained activated after alcohol withdrawal. The top hit was CCAAT enhancer binding protein beta (C/EBPβ). We found that hepatocyte-specific Cebpb knockout at the time of alcohol cessation promoted fibrosis resolution. The resolution was mediated by altered hepatocyte-macrophage crosstalk. C/EBPβ suppressed the expression of CYP3A family of enzymes in hepatocytes and downstream macrophage collagen degradation ability. Cebpb knockout in hepatocytes promoted a proresolving phenotype in liver macrophages. We further identified upstream events leading to persistent C/EBPβ activation. C/EBPβ was induced by alcohol-mediated endothelial changes during ALD development and resolution. Restoring endothelial cell function with angiopoietin-1 supplementation reduced C/EBPβ and promoted fibrosis resolution. CONCLUSIONS: Taken together, alcohol-induced C/EBPβ activation is a key driver of poor disease resolution in ALD and a promising target for patients who fail to recover after alcohol abstinence.

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  • Hepatocyte-specific deletion of C/EBPβ at the time of alcohol cessation induces a pro-resolutive macrophage phenotype during alcohol-associated liver disease.

    “while hepatocyte-specific deletion of C/EBPβ at the time of alcohol cessation induces a pro-resolutive macrophage phenotype during alcohol-associated liver disease, highlighting the importance of hepatocyte–macrophage crosstalk (79).”

    From Strategies to promote liver fibrosis amelioration with involvement of restorative macrophages (2026) · cites this paper as [79]

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Cited by

Sorted by citations

Authors
Schonfeld, M., Nataraj, K., Mah, S., Weinman, S., & Tikhanovich, I.
Affiliations
University of Kansas Medical Center (US)
Corresponding author
Tikhanovich, Irina
ORCID
Venue
Cellular and Molecular Gastroenterology and Hepatology
Publisher
Elsevier BV
Published
2025
Volume
19
Issue
9
Pages
101525
ISSN
2352-345X (ISSN-L)
DOI
10.1016/j.jcmgh.2025.101525
PMC
PMC12206133
OpenAlex
W4409829112
Cited by
5
References
0
Citations by year
2026: 3 · 2025: 2
FWCI
2.81
Type
journal article
Language
en
Open access
Licence
Locations
  • Cellular and Molecular Gastroenterology and Hepatology (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
Funders
  • National Institute on Alcohol Abuse and Alcoholism
  • Samson
  • National Institutes of Health National Institute of Allergy and Infectious Diseases (AI178204)
  • U.S. Department of Veterans Affairs (I01BX004694)
Topics
  • Health Sciences › Medicine › Hepatology › Liver physiology and pathology
  • Health Sciences › Medicine › Pathology and Forensic Medicine › Alcohol Consumption and Health Effects
  • Health Sciences › Medicine › Epidemiology › Liver Disease Diagnosis and Treatment
Keywords
C/EBPβ, alcoholic liver disease, alcohol abstinence, collagen degradation, angiopoietin-1, endothelial dysfunction, hepatocyte-specific knockout, transcription factor activation, single-cell ATAC-seq
MeSH terms
Ethanol, Animals, Disease Models, Animal, Humans, Liver, Liver Cirrhosis, Alcoholic, Macrophages, Male, Mice, Inbred C57BL, Mice, Knockout, Hepatocytes, CCAAT-Enhancer-Binding Protein-beta, Angiopoietin-1, Endothelial Cells, Mice, Diet, High-Fat, Alcohol Abstinence

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